Danger, bacteria at work - making you fat!

[JRStern]

http://www.newscientist.com/article/mg21628964.700-blame-bacteria-if-you-start-putting-on-weight.html

Blame bacteria if you start putting on weight
19 December 2012
Magazine issue 2896.

WEIGHT gain bugging you? Evidence is mounting for the central role
that bacteria play in causing obesity.

Liping Zhao and his team at Shanghai Jiao Tong University in China put
a morbidly obese man on a diet of whole grains, traditional Chinese
medicines, probiotics and non-digestible carbohydrates for 23 weeks.
The diet was designed to inhibit the bacteria thought to be associated
with weight gain by increasing the pH in the colon.

The 175-kilogram volunteer lost 51 kg, despite not exercising. People
who have had weight-loss surgery lose on average 49 kg.

To see if the bacteria present also changed, the team looked at what
species were prevalent in the volunteer's gut before and after the
diet. Before the regime, Enterobacter - a toxin-producing pathogen -
was most abundant, accounting for 35 per cent of the gut bacteria.
After the diet, it was reduced to undetectable levels.

The researchers fed mice samples of this bacterium from the
volunteer's gut to determine whether the pathogen was a cause or a
result of his obesity. They found that the mice with the new bacteria
gained significantly more weight on a high fat diet than control mice,
also on a high fat diet (International Society for Microbial Ecology,
doi.org/jz9).

Previous work has shown a link between gut bacteria and obesity, but
Zhao describes this as "the last missing piece of evidence that
bacteria cause obesity". Treatment with an appropriate diet could be
cheaper and more effective than surgery, he says.

[randall]

On Dec 19, 10:07 pm, JRStern <JRSt...@foobar.invalid> wrote:
> http://www.newscientist.com/article/mg21628964.700-blame-bacteria-if-...

Jxr.

So? Why not blame the bacteria from MOM 1st, then?

Fat or lean you know what i MEAN?

Lactobacillus Johnsonii - 9 hits - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=Lactobacillus+Johnsonii+&start=0&

Shall i save the BEST for last?

me me me... or bb bb bb ?

Wow me and BB?

The Big BANG! I will put something together in the END times...

so reverse BB? Or how the universe unfolds or inverse with a reverse?

Hey this is little BUG thread now..

But i luv long posts and long TIME universe or multi verse for that
matter, which means
we don't require re-incarnations. LOL

Ok ok...

And thus prevent the ADD crowd like ADAM LANZA and hpa-axis sally from
making it to the END of this video game?

Er er er Thread or this post to be specific.

Oh wait.. he as in ADAM and not eve, ended his space odyssey! You'd
think he had low vitamin D3 and
being vegan (low copper) and <i'll do a short post on him and contrast
it to us?>


what psor heads don't go postal and have a prefrontal cortex and
limbic malfunction?

hey move on dot dork... ok

sure.. bu but but..

Big deal and if i instruct hpa-axially Susan to read the haPPy ending
first, she DOES. <g>

So there you go...READ the happy ending and then decide if you want to
evolve in this
or any universe? LOL

OK being on TRACK now... jack:

But, but.. for the mice in that Liping Zhao trial..

being Obese is pure happiness.. in spades.. no less. <g> <w>

Didn't BEING fatty patty in TCM land mean you had some spending CASH
versus
topping off with high fructose these days and even poor people can be
FAT and moronish and vote for a f minus (economics and foreign
affairs) preezy dent? LOL .

How the TIMES change!

So... Schumpeterian i know!

http://en.wikipedia.org/wiki/Creative_destruction
http://en.wikipedia.org/wiki/Joseph_Schumpeter%23Schumpeter_and_capitalism.27s_demise

Wow.. that was a curve ball i didn't see COMING... is hpa susan still
reading
or did she go straight for the FAT fast ball over the middle of the
PLATE?

Pass the prime rib! <g>


ok ok.. this is your id squid.. and stick to the FAT now.. LOL

It's a meaty question ALL right! .. LOL

sorry id squid.. you being a basic instinct are most likely stucky
pooh like adam lazer beam? LOL

sugar sugar, honey honey? And BAD versus GOOD!

How much fructose did adam consume for that smarty farty brain of his?

Not to mention an enterotypes expose! <g>

And for most psor heads a test of quality versus quantities!

And this TIME i mean the meat and not to demean those who don't EAT
it. LOL

No wonder BB is getting so CLEAR, you'd think? <w>

But what about skinny benny adam lanza who i heard was vegan then?

Another question and not for NOW, but stuck in me gulliver..
(clockwork orange -nadsat speak)

Give me the MEAT: (er er er money? ) LoL

How many hits for ME and

___Enterobacteria___ randall psoriasis- ALL GROUPs?
Whoops: only 10.. (LoL)
https://groups.google.com/groups/search?q=Enterobacteria+randall+psoriasis&btnG=Search&sitesearch=


As i'm not so enterotypicow..moo mooo he eats them! i'll do it in the
p ng just to see who was FIRST.

But but.. i was doing a fecal transplant (wit kit - webster implant
technique) before these monkey's even knew what it meant.. LOL

11 hits: enterobacter - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=Enterobacter&start=0&


hit #1 of 11:

ron gorgichuk said:

: Wed, Mar 7 2001 7:09 am
Subject: Re: Probably a stupid question
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/e3f4f77a1b704933


[...] Associated organisms thought to provoke a psoriatic attack were
as follows:
streptococcal groups A, B, C, D, F, G, S viridans, S pneumoniae;
Klebsiella
pneumoniae, oxytoca; Escherichia coli;_____ Enterobacter ____ loacae,
E aerogenes, E
agglomerans; Proteus mirabilis, P vulgaris; Citrobacter freundii, C
diversus; Morganella morganii; Pseudomonas aeruginosa, P maltiphilia,
P
putida; Serratia marcescens; Acinetobacter calbio aceticus, A luoffi;
Flavobacterium specie; CDC groups Ve-1, Ve-2, E-o2; Bacillus
subtilis,
cereus; Staphylococcus aureus; Candida albicans, C parapsilosis;
Torulopsis,
glabrata; Rhodotorula and dermatophytes.
One or more antistreptococal enzyme tests was positive in 50% of
patients.
Titers to hepatitis E were elevated in one patient and to HIV in two
patients.
<snip>

So what's the POOP?

My smart rear end comments: (previous to the above but same thread &
most illuminating. LOL)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/025657dc4c6be375
<snip>

Gosh i nailed it before most knew that raising pH in the colon
(slightly acidic BTW) was KEY. <w>

me me me... clearing his ... gullet and wait till the FAT lady
sings.. ring a ding ding!

And hit #2 is evetsm to will brittian harrison on Nov 30 of 1999
1999/11/30
Subject: Re: beta-carotene, carrots, tomatoes, fresh fruit
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/4bebe66c0271d14d/6c260415707dbee8?lnk=gst&q=Enterobacter#6c260415707dbee8

Which says diet is doing what your scientist article says and does
also mention ENTERoBACTER:
<snip>

LOL

But i like the two at the END. Mine.

LOL
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/e8fac1cda6403a38/ad6100557811f412?lnk=gst&q=Enterobacter#ad6100557811f412
Fri, Jan 14 2011 11:17 am
Subject: ABstracts -- SFB->Th17 - CPG Islands in PSOR STREAM - CCR6 -
A20 - IL23 - Byron Links - Gut Microbes RISING? TLR2 or TLR* -
Cardiation & Bugs - +++

[...] http://www.medicalnewstoday.com/articles/212957.php
[...] In the paper, researchers describe processing the tissue using
cell cultures and genomic analysis to look for the presence of
culturable bacteria. In addition, they looked at five pairs of
diseased and healthy arterial tissue. The use of cell cultures aided
in the isolation of the bacillus Enterobacter hormaechei from the
patient's tissue. Implicated in bloodstream infections and other
life-
threatening conditions, the isolated bacteria were resistant to
multiple antibiotics. Surprisingly, using quantitative methods, this
microbe was further identified in very high numbers in diseased but
not in healthy arterial tissues.
The data suggest that a chronic infection may underlie the process of
atherosclerosis, an infection that can be initiated by the systemic
dissemination of bacteria though different "gates" in the vascular
wall - as in the case of a septic patient, through intestinal
infection. The data support Dr. Kozarov's previous studies, where his
team identified periodontal bacteria in carotid artery, thus pointing
to tissue-destructing periodontal infections as one possible gate to
the circulation.
<snip>


https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/2392d86d19f39d75/86068fe572aee4fa?lnk=gst&q=Enterobacter#86068fe572aee4fa
Wed, Jan 12 2011 4:57 pm
Subject: Hearts with SOUL? - Psor ABstractions --Autoimmune ODDs (SEE
PsA!)- SFB/Th17/& more -FoxP3 & TREGs - Plantarum & Kimchi - Aspirin -
DEFA5 & Crohn's- DRD4 SnP - Crazy MAN why? -IL-10 Th2 Skew? - Gut
Microbiota redux -

[...] http://en.wikipedia.org/wiki/Human_flora#Gut_flora
[...] Bacteria make up most of the flora in the colon[25] and 60% of
the dry mass of feces.[22] This fact makes feces an ideal source to
test for gut flora for any tests and experiments by extracting the
nucleic acid from fecal specimens, and bacterial 16S rRNA gene
sequences are generated with bacterial primers. This form of testing
is also often preferable to more invasive techniques, such as
biopsies. Somewhere between 300[22] and 1000 different species live
in
the gut,[20] with most estimates at about 500.[23][26] However, it is
probable that 99% of the bacteria come from about 30 or 40 species.
[27] Fungi and protozoa also make up a part of the gut flora, but
little is known about their activities.

Research suggests that the relationship between gut flora[28] and
humans is not merely commensal (a non-harmful coexistence), but
rather
is a mutualistic, symbiotic relationship.[20] Though people can
survive with no gut flora,[23] the microorganisms perform a host of
useful functions, such as fermenting unused energy substrates,
training the immune system, preventing growth of harmful species,[22]
regulating the development of the gut, producing vitamins for the
host
(such as biotin and vitamin K), and producing hormones to direct the
host to store fats. However, in certain conditions, some species are
thought to be capable of causing disease by causing infection or
increasing cancer risk for the host.[22][25]

Some bacteria found in the large intestine of humans:
Bacterium--------- --------Range of Incidence
Bacteroides fragilis-------- 100
Bacteroides melaninogenic---- 100
Bacteroides oralis -----------100
Lactobacillus ----------------20-60
Clostridium perfringens -------25-35
Clostridium septicum--------- 5-25
Clostridium tetani------------ 1-35
Bifidobacterium bifidum -------30-70
Staphylococcus aureus------ 30-50
Enterococcus faecalis--------- 100
Escherichia coli --------------100
Salmonella enteritidis--------- 3-7
Klebsiella sp.-------------- 40-80
Enterobacter sp.------------ 40-80
Proteus mirabilis--------------- 5-55
Pseudomonas aeruginosa --------3-11
Peptostreptococcus sp.----------- ?common
Peptococcus sp. ?common
<snip>

==============

Where or which one is the sFB in the gut that inducts or id sucks the
Th17?

see
PMID: 19836068

Induction of intestinal Th17 cells by segmented filamentous bacteria.
Ivanov II, Atarashi K, Manel N, Brodie EL, Shima T, Karaoz U, Wei D,
Goldfarb KC, Santee CA, Lynch SV, Tanoue T, Imaoka A, Itoh K, Takeda
K, Umesaki Y, Honda K, Littman DR.
Cell. 2009 Oct 30;139(3):485-98. doi: 10.1016/j.cell.2009.09.033.
http://www.ncbi.nlm.nih.gov/pubmed/19836068

And another DANGER will Robinson! ALERT!

BB will go postal and do the inverse of the big bang. LOL

================= wait .. back to me me me

But of course we get 10 hits for ALL groups:
This time:

Enterobacter enterotypes- all groups ( 4 of TEN are MINE)
https://groups.google.com/groups/search?q=Enterobacter+enterotypes&btnG=Search&sitesearch=

So enterobacter comes up as Enterobacteria and Enterobacteriaceae
family etc.

And we get 22 hits : Enterobacteria - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=Enterobacteria&start=0&

and ODDLY enough if you add me to this search:

We get more then 22 hits (picks up similars you think? <w>)

Like : enterobacteria and enterobacter and Enterobacteriaceae etc..

40 results for Enterobacteria randall - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=Enterobacteria+randall&start=0&

40 hits and all me me me.. LOL

So how randall goes postal on bad bacteria. Coming up his craw
daddy...!

How brown COW?

Is easy.. check BAD bacteria and ME... fat lady? No no... not this
time.

Why have her horn in on my PORK chops (high copper + iron and xyz's,
though!) ? LOL

Put it in chop suey please.. <w> chop chop!

Wow ONLY 54 hits for me and BAD bacteria - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=BAD+bacteria+randall&start=0&

But but butt hole.. i'm feeling it...

is it the BiG piG BANG... working it's way up or down? LOL

Or the pi in your eye?

...

Whoops.


Boom!

573 hits for BAD Flora and ME!

LOL

wow.. i save the BEST for LAST..

How prescient?

573 results for BAD Flora randall- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=BAD+Flora+randall&start=0&



Wow.. this is a good versus BAD thingy pooh and inside of YOU.

Gosh..

Enterotypes and SFB does mean something..

You need a pmid on that one? LOL

or slightly acidic colon?

122 hits: slightly acidic colon randall psoriasis- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=slightly+acidic+colon+randall+psoriasis&start=0&

Gosh you can eat meat and drink a glass of red wine and smoke one cig
(hormesis) and still live to 122 like Jeanne Calment
if you ALSO exercise.


http://en.wikipedia.org/wiki/Hormesis

http://en.wikipedia.org/wiki/Jeanne_calment#Health_and_lifestyle

And don't forget the OLIVE oil.. LOL

so popeye can share some spinach!

But... isn't there to MUCH meat in this post as my cat is scratching
me for attention?

LOL

she's killing birds like adam lanza... i seeded the grass after
we got an inch and a half of rain..

and those cute little baby birds are coming in to a veritable TRAP.

And then coco kills THEM.

Is that in her LIMBIC brain?

How come she kills them but doesn't EAT them?

You take them away you nit wit?

Right id squid.. i do

ido... indoleamine. i'm so mean!


randall.. Primum non nocere oh oh oh i've got a quote for BB now?

[JRStern]

On Thu, 20 Dec 2012 10:43:26 -0800 (PST), randall <ranh...@aol.com>
wrote:

>Some bacteria found in the large intestine of humans:
>Bacterium--------- --------Range of Incidence
>Bacteroides fragilis-------- 100
>Bacteroides melaninogenic---- 100
>Bacteroides oralis -----------100
>Lactobacillus ----------------20-60
>Clostridium perfringens -------25-35
>Clostridium septicum--------- 5-25
>Clostridium tetani------------ 1-35
>Bifidobacterium bifidum -------30-70
>Staphylococcus aureus------ 30-50
>Enterococcus faecalis--------- 100
>Escherichia coli --------------100
>Salmonella enteritidis--------- 3-7
>Klebsiella sp.-------------- 40-80
>Enterobacter sp.------------ 40-80
>Proteus mirabilis--------------- 5-55
>Pseudomonas aeruginosa --------3-11
>Peptostreptococcus sp.----------- ?common
>Peptococcus sp. ?common
><snip>
>
>==============
>
>Where or which one is the sFB in the gut that inducts or id sucks the
>Th17?

I dunno, but getting back to fat, the thing is whatever the germ is
making can be countered in the gut or after.

Heck, it might also have positive uses, like keeping cancer patients
nourished or something.

J.

[randall]

On Dec 20, 6:10 pm, JRStern <JRSt...@foobar.invalid> wrote:
> On Thu, 20 Dec 2012 10:43:26 -0800 (PST), randall <ranhu...@aol.com>

jxr

Hey.. that enterobacter thingy is cool and indicts the gut flora
that goes pow on it inside of us. But that is still controlled
by sunshine D3 and extra TREGs in the colon no doubt. LOL

So ... go vegan-ish in the winter and drink egg nogg? <g>


and it all goes with nature yesterday.

Just noticed

some of nature stuff came out on pubmed today

---

Therapeutics: Silencing psoriasis.
Crow JM.
Nature. 2012 Dec 20;492(7429):S58-9. doi: 10.1038/492S58a. No abstract
available.
PMID: 23254974 [PubMed - in process]

3.
Psoriasis uncovered.
Crow JM.
Nature. 2012 Dec 20;492(7429):S50-1. doi: 10.1038/492S50a. No abstract
available.
PMID: 23254970 [PubMed - in process]

4.
Psoriasis.
Grayson M.
Nature. 2012 Dec 20;492(7429):S49. doi: 10.1038/492S49a. No abstract
available.
PMID: 23254969 [PubMed - in process]

-----

And this Grayson Michelle hit has a nice: link to microbiome stuff.

http://www.nature.com/nature/journal/v492/n7429_supp/full/492S49a.html
Psoriasis

Michelle Grayson
Nature 492, S49 (20 December 2012) doi:10.1038/492S49a
Published online 19 December 2012

After decades of modest advances, psoriasis research has caught fire.
In the past ten years, immunosuppressant drugs developed for other
autoimmune diseases, such as rheumatoid arthritis, have had a powerful
effect in treating severe cases. What's more, this success underscores
the crucial role the immune system plays in psoriasis — and points to
new ways to treat this inflammatory skin disease. Digging deeper into
the underlying causes of psoriasis has unearthed a host of new drug
targets. And several promising treatments are nearing clinical
approval (see page S58).

Building on this knowledge, genetic studies have provided clues to
which parts of the immune system have gone awry in psoriasis — and
hinted at where this enigmatic disease might start (S56).

Indeed, psoriasis has become something of a therapeutic test bed for
other immune-mediated and inflammatory conditions. Its visible plaques
are easy to measure and biopsy to assess treatment efficacy (S50).
Psoriasis research has shown the skin to be a vibrant, immunologically
active organ (S52). And the skin is home to a variety of microbial
communities — disturbances in the skin microbiome may well be what
opens the door to psoriasis in the first place (S60).
<see link below for s60>

Although its most obvious impact is on the skin, psoriasis runs deep.
Patients are at increased risk of cardiovascular disease, have a
higher incidence of metabolic syndrome, and often get psoriatic
arthritis. Dermatologist Henning Boehncke outlines the implications of
these effects on general healthcare (S55). Psoriasis takes a
psychological toll too. In certain individuals, stress can cause the
disease to flare up (S62), but holistic treatments using cognitive
behavioural therapy seem to help (S64).

We acknowledge the financial support of Celgene in producing this
Outlook. As always, Nature has full responsibility for all editorial
content.
<snip>


<S60>
http://www.nature.com/nature/journal/v492/n7429_supp/full/492S60a.html
Microbiome: The surface brigade

Bijal Trivedi
Nature 492, S60–S61 (20 December 2012) doi:10.1038/492S60a
Published online 19 December 2012

<and great images also so use the above link>

Our skin is home to thousands of species of bacteria — and when these
microscopic societies are disrupted, skin infections can arise.

Subject terms:
Skin manifestations Psoriasis Microbiome

Each one of us is home to some 100 trillion bacteria. This mass of
microbes — accounting for 1–3% of our body weight — resides in our
mouth, nose, genitals and intestines, as well as on our skin. Although
we are only just beginning to discover what these microscopic
hitchhikers do, it is already obvious they are not freeloaders — many
play an important role in maintaining human health. There is even
preliminary evidence1 suggesting that when we eradicate certain
species of bacteria or alter their relative populations, we
inadvertently contribute to the development of diseases ranging from
obesity to asthma.

Determining the identity and roles of these microorganisms is the goal
of the Human Microbiome Project. In June 2009, scientists from the
project released a survey2 of microbes dwelling at 20 locations on the
skin of the human body. This census, based on 10 healthy volunteers,
produced two significant results, says Julie Segre, a leader of the
skin microbiota sequencing efforts at the National Human Genome
Research Institute in Bethesda, Maryland. First, it revealed the
diversity of microbes that reside on healthy skin. Second, it showed
that the organisms varied depending on whether the area was oily like
the chest; moist, as in the armpit; or dry, like the forearm (see
'Microbiome map').

map
http://www.nature.com/nature/journal/v492/n7429_supp/images/492S60a-i2.0.jpg

Just as the microbes in the gut provide nutritional benefits, those on
the skin also earn their keep. Some have evolved to eat dead skin,
some transform the oils that skin cells produce into a natural
moisturizer, and others are thought to keep harmful bacteria and
viruses from invading. And in the past few years investigators,
including Segre, have started to explore whether an imbalance in
microbes contributes to skin diseases such as psoriasis and eczema.

Skin survey
Martin Blaser, a microbiologist at New York University's Langone
Medical Center, became interested in psoriasis almost a decade ago
after personally developing a mild case. As a physician specializing
in infectious diseases, Blaser was well aware of the skin's contingent
of normal flora, and wondered whether a change in these microbes had
triggered his disease. He investigated this question and in 2007
published one of the earliest surveys of microbes living on the human
forearm. Following the launch of the Human Microbiome Project in
December 2007, he received a grant from the US National Institutes of
Health to further explore the link between microbes and psoriasis
along with his then colleague, dermatologist Bruce Strober.

Psoriasis, which typically causes red, raised, scaly, itchy plaques,
affects about 2–3% of the world's population (see 'Psoriasis
uncovered', page S50). Although Blaser's case was mild, the disease
can be debilitating. Those most severely affected “can be among the
most miserable patients on Earth”, says Strober, now at the University
of Connecticut in Farmington. Blaser's team in New York examined the
microbes inhabiting the lesions of psoriasis patients. Using a damp
cotton applicator, Strober swabbed the plaques for a bacterial sample.
Then he took another sample from the patient's healthy skin. He also
collected microbes from patients with no signs of the disease.

Blaser discovered3 that the cast of microbes inhabiting the plaque is
much more diverse than on healthy skin from either psoriatic or
unaffected individuals. He also found that the major phyla of bacteria
were present on both psoriatic and healthy skin, but in different
ratios. Most notably, there was a striking trend in bacteria from the
Proprionibacterium genus: healthy skin had most, unaffected skin from
psoriasis patients had moderate levels, and psoriatic lesions
contained least.

This was a small study, says Strober, and it's far from clear whether
these differences are a “cause, effect or correlation”. Although he
admits that “this issue is in its infancy”, he is convinced there is a
microbial component to psoriasis. One clue, Strober says, comes from
identical twins: in 70% of cases, both suffer from the disease.
“That's proof that the environment plays a part and it's not all
genetic,” he explains. What's more, he says, the unexpected flare-ups
that characterize the disease might be set off by environmental
triggers that alter the composition of the skin's microbe population.

Blaser, meanwhile, has expanded the study and will submit results for
publication at the end of 2012. The data suggest there is no single
organism that is present in the psoriatic lesions but not on healthy
skin, so there is unlikely to be an obvious microbial villain to
exterminate. “It's going to be more complicated,” he says.

The link between microbes and psoriasis is still unproven. “It's early
days,” says Frank Nestle, a skin immunologist and dermatologist at
King's College London. Nestle is taking an active role in exploring
this association as leader of the UK arm of a US$6.5-million
international consortium to probe the skin microbiome. The project,
Microbes in Allergy and Autoimmunity Related to the Skin (MAARS), aims
to identify the microorganisms that protect against allergy and
autoimmune diseases, as well as the pathogenic bacteria that trigger
them. MAARS will focus on the two most prevalent chronic inflammatory
skin diseases: eczema and psoriasis.

Surface issues
Research on the skin microbiome lags behind that of the gut
microbiome. Nevertheless, there are signs that skin microbes play a
crucial role in overall health. In 2012, Yasmine Belkaid, an
immunologist at the US National Institute of Allergy and Infectious
Diseases in Bethesda, described4 a link between the microbes on the
skin and the body's ability to mount a robust immune response. Belkaid
discovered that mice raised in sterile chambers, lacking bacteria on
the skin, in the gut and elsewhere, were unable to fight off the
parasite Leishmania major. However, if the germ-free mice were
inoculated with Staphylococcus epidermidis — a common skin microbe on
mice and humans — at the same time as the L. major infection, they
were able to defeat the parasite.

Belkaid discovered that S. epidermidis interacts with T cells in the
skin to produce inflammatory molecules that are central to the immune
response. “It's possible that other bacteria on the skin can also
rescue this immune response,” says Belkaid, “but the point is that
there is a link between the community of microorganisms on the skin
and the animals' ability to protect against harmful microbes.” If a
lack of microbes on the skin cripples the immune system, she adds,
then it's not unreasonable to think that disrupting the skin's
microbial communities might leave it vulnerable to disease.

The evidence linking the microbiota and eczema, which affects more
than 15% of children and 2% of adults in the United States, is more
solid than for psoriasis. The number of children suffering from eczema
has tripled in industrialized nations in the past 30 years, suggesting
an environmental trigger. Research has shown5 that more than 90% of
eczema patients have colonies of Staphylococcus aureus on both their
affected and unaffected skin. In contrast, the microbe is rarely
present on healthy people. Segre adds that, in contrast to psoriatic
lesions, eczema sores tend to have a much lower diversity of bacteria
than healthy skin. What's more, as the condition worsens, S. aureus
will often overwhelm the whole microbial community.

Proven treatments for eczema include topical antibiotics, steroids and
mild bleach baths. But there are no effective antimicrobial treatments
for psoriasis. That might seem like a strike against the link between
microbes and psoriasis. But, says Blaser, history teaches us not to be
so quick to dismiss such an idea. Early efforts to treat gastritis
with antibiotics failed, arguing against a bacterial cause. It wasn't
until Barry Marshall and Robin Warren discovered Helicobacter pylori
in the stomachs of patients suffering from inflammation and ulcers
that it became possible to develop a targeted regimen — two or three
antibiotics plus an acid suppressant — that eradicated the specific
bacterium and cured patients.

In a parallel with Blaser's hypothesis about psoriasis, Segre says it
is unlikely that S. aureus alone leads to eczema. “We have to move
away from the idea that one bacterium causes one disease,” she says.
“It's going to be much more subtle.” Blaser and Segre suspect that
diseases such as eczema and psoriasis might instead be related to a
shift in the balance of microscopic skin-dwellers. “The challenge is
to find out whether there's a causal link between a disturbance in the
microbiome and a particular disease,” says Blaser.

Future psoriasis therapies, ____Blaser_____ suggests, might include
ointments and creams spiked with particular bacteria that block the
growth of other harmful bacteria, or that interact with the immune
system to boost its ability to heal skin lesions and maintain skin
health.

Whatever eventual treatments come from this work, it is increasingly
apparent that our skin is not the first line of defence against the
external world: that role falls instead to the army of microbes that
live there. Keeping them happy could be the key to keeping our skin
soft, supple and healthy.

References
<snip>

So the blaser cream would balance strep and staph or what?

-----

Author of this nature article: Trivedi gets 3 hits on the p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=Trivedi&start=0&

31 hits for (creamy DREAMY->>) BLASER (hit #1 is with LITTMAN> p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=blaser&start=0&

5 of 31 blaser hits have littman: p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=blaser+littman&start=0&scoring=d&


OK.. the mayan thing is a bore. LOL

randall.. xmas gifts are stolen by a grinch... named psorHEAD... LOL

[JRStern]

On Fri, 21 Dec 2012 13:29:53 -0800 (PST), randall <ranh...@aol.com>
wrote:

>Psoriasis, which typically causes red, raised, scaly, itchy plaques,
>affects about 2–3% of the world's population (see 'Psoriasis
>uncovered', page S50). Although Blaser's case was mild, the disease
>can be debilitating. Those most severely affected “can be among the
>most miserable patients on Earth”, says Strober, now at the University
>of Connecticut in Farmington.

Amen.

I'm not quite there but I can see it from here, and if I stopped
taking the curcumin I think I would be a contender inside of week.

J.

[randall]

On Dec 21, 5:05 pm, JRStern <JRSt...@foobar.invalid> wrote:
> On Fri, 21 Dec 2012 13:29:53 -0800 (PST), randall <ranhu...@aol.com>

jxr

But would we see it in your eyes?

Or debilitations? Due to four times more inflammation
thanks to card14 mutation or it's snp thingy?

And we all have something dietarEALLY that we believes WORKs.

Like artichoke hearts or broccoli or fill in the blank __+_____.

If i stop using longevinex.com i'm SLOWER and it was
longevinex.com that took me away from curcumin when those
personal trials began.

And as Longevinex affects 1711 genes i'm hoping one of
those gives us the ultimate CLUE.

Do they all come back to ONE gene that ties all autoimmune
conditions together?

Is it mhc or upstream? Or maybe just a copy number polymorphism?

http://en.wikipedia.org/wiki/Major_histocompatibility_complex#Class_II

OK..or a combo of I + III or II? + a virus or bacteria (staph or strep
or candida or er")

Certainly activated inflammatory genes MUST turn the
lively living ones (makes you thus!!) Down?

OK the eyeball thing i noticed a few days ago.

Where did it go go?

Found it:


MS it's in yOUR eye balls?

huh?

How much ms you've got that is!

What?


http://www.bbc.co.uk/news/health-20836082
Simple eye scan can reveal extent of Multiple Sclerosis

12/24/12

----

see
http://news.bbcimg.co.uk/media/images/64932000/jpg/_64932318_eye-spl-1.jpg
The retina sits at the back of the eye and houses the cells that
provide us with vision

-----

A simple eye test may offer a fast and easy way to monitor patients
with multiple sclerosis (MS), medical experts say in the journal
Neurology.

Optical Coherence Tomography (OCT) is a scan that measures the
thickness of the lining at the back of the eye - the retina.

It takes a few minutes per eye and can be performed in a doctor's
surgery.

In a trial involving 164 people with MS, those with thinning of their
retina had earlier and more active MS.

The team of researchers from the Johns Hopkins University School of
Medicine say larger trials with a long follow up are needed to judge
how useful the test might be in everyday practice.

The latest study tracked the patients' disease progression over a two-
year period.

Unpredictable disease

Multiple sclerosis is an illness that affects the nerves in the brain
and spinal cord causing problems with muscle movement, balance and
vision. In MS, the protective sheath or layer around nerves, called
myelin, comes under attack which, in turn, leaves the nerves open to
damage.

There are different types of MS - most people with the condition have
the relapsing remitting type where the symptoms come and go over days,
weeks or months.

Usually after a decade or so, half of patients with this type of MS
will develop secondary progressive disease where the symptoms get
gradually worse and there are no or very few periods of remission.

Another type of MS is primary progressive disease where symptoms get
worse from the outset.

There is no cure but treatments can help slow disease progression.

It can be difficult for doctors to monitor MS because it has a varied
course and can be unpredictable.

Brain scans can reveal inflammation and scarring, but it is not clear
how early these changes might occur in the disease and whether they
accurately reflect ongoing damage.

Scientists have been looking for additional ways to track MS, and
believe OCT may be a contender.

OCT measures the thickness of nerve fibres housed in the retina at the
back of the eye.

Unlike nerve cells in the rest of the brain which are covered with
protective myelin, the nerve cells in the retina are bare with no
myelin coat.

Experts suspect that this means the nerves here will show the earliest
signs of MS damage.

The study at Johns Hopkins found that people with MS relapses had much
faster thinning of their retina than people with MS who had no
relapses. So too did those whose level of disability worsened.

Similarly, people with MS who had inflammatory lesions that were
visible on brain scans also had faster retinal thinning than those
without visible brain lesions.

Study author Dr Peter Calabresi said OCT may show how fast MS is
progressing.

"As more therapies are developed to slow the progression of MS,
testing retinal thinning in the eyes may be helpful in evaluating how
effective those therapies are," he added.

In an accompanying editorial in the same medical journal that the
research is published in, MS experts Drs Robert Bermel and Matilde
Inglese say OCT "holds promise" as an MS test.
<snip>


And i found peter's abstract.

kewl.. but is he related to Janet? LOL

now i'm having FUN instead of a COW. <w>


http://www.ncbi.nlm.nih.gov/pubmed/23267030
Neurology. 2013 Jan 1;80(1):47-54.
Active MS is associated with accelerated retinal ganglion cell/inner
plexiform layer thinning.

Ratchford JN, Saidha S, Sotirchos ES, Oh JA, Seigo MA, Eckstein C,
Durbin MK, Oakley JD, Meyer SA, Conger A, Frohman TC, Newsome SD,
Balcer LJ, Frohman EM, Calabresi PA.

Source
From the Department of Neurology (J.N.R., S.S., E.S.S., J.A.O.,
M.A.S., C.E., S.D.N., P.A.C.), Johns Hopkins University School of
Medicine, Baltimore, MD; Department of Neurology (C.E.), University of
South Alabama College of Medicine, Mobile; Carl Zeiss Meditec Inc.
(M.K.D., J.D.O., S.A.M.), Dublin, CA; Voxeleron LLC (J.D.O.), San
Francisco, CA; Department of Neurology and Ophthalmology (A.C.,
T.C.F., E.M.F.), University of Texas Southwestern, Dallas; and
Department of Neurology and Ophthalmology (L.J.B.), University of
Pennsylvania, Philadelphia.

Abstract
OBJECTIVE:
To determine the effect of clinical and radiologic disease activity on
the rate of thinning of the ganglion cell/inner plexiform (GCIP) layer
and the retinal nerve fiber layer in patients with multiple sclerosis
(MS) using optical coherence tomography (OCT).

METHODS:
One hundred sixty-four patients with MS and 59 healthy controls
underwent spectral-domain OCT scans every 6 months for a mean follow-
up period of 21.1 months. Baseline and annual contrast-enhanced brain
MRIs were performed. Patients who developed optic neuritis during
follow-up were excluded from analysis.

RESULTS:
Patients with the following features of disease activity during follow-
up had faster rates of annualized GCIP thinning: relapses (42% faster,
p = 0.007), new gadolinium-enhancing lesions (54% faster, p < 0.001),
and new T2 lesions (36% faster, p = 0.02). Annual GCIP thinning was
37% faster in those with disability progression during follow-up, and
43% faster in those with disease duration <5 years vs >5 years (p =
0.003). Annual rates of GCIP thinning were highest in patients
exhibiting combinations of new gadolinium-enhancing lesions, new T2
lesions, and disease duration <5 years (70% faster in patients with vs
without all 3 characteristics, p < 0.001).

CONCLUSIONS:
MS patients with clinical and/or radiologic nonocular disease
activity, particularly early in the disease course, exhibit
accelerated GCIP thinning. Our findings suggest that retinal changes
in MS reflect global CNS processes, and that OCT-derived GCIP
thickness measures may have utility as an outcome measure for
assessing neuroprotective agents, particularly in early, active MS.

PMID: 23267030

And check out the conclusions here:

http://www.ncbi.nlm.nih.gov/pubmed/22836772

[...] Thinner GC-IPL was independently associated with older age,
female sex, longer axial length, and thinner RNFL thickness. These
factors should be taken into account when interpreting GC-IPL
thickness measurements with HD-OCT for glaucoma assessment.

PMID: 22836772


Are there a few gene's here spelling out a question?

Don't know.

31 hits : gcip -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=gcip

11 of 31 and #2 is Chlamydia (PMID: 17532760 )
http://www.ncbi.nlm.nih.gov/pubmed?term=gcip%20gene

and Psoria* + eye - 281 hits
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20eye

10 of these have eye and hit #1 is at the downunder EYE research

so

http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20eye%20gene

And hit #1 is PMID: 22837109

And PMID: 22837109 was posted here on august

I emember NOW it was HOT that day. LOL

Global warming i'm guessing?

you'd think? With 8 zillion people burning Carbon to stay warm.

We'd switch to nuclear zitulation fuel and pop them?

Oh no we can't pop a zit to stay WARMER that will KILL mother earp.
LOL

Kewl show on the SUN last night.. but i missed it. I was watching
WWJD or southpark

http://en.wikipedia.org/wiki/A_Scause_for_Applause

[...] Plot

The town of South Park discontinues using their "What would Jesus do?"
bracelets after learning that traces of performance-enhancing drugs
and other illicit substances were found on the Shroud of Turin,
leading to the conclusion that Jesus did not suffer for humanity's
sins or perform miracles of his own ability, but was merely under the
influence of drugs.
<snip>

ok not really but i wanna! Will barackOHclaus make episodes FREE?

Just for ME?

I'm voting like a moron now.. LOL

Wait a minute...

OK on that HOT day in august:

Tues, Aug 7 2012 11:13 am
Subject: Strange BREW (Lavender) - Nestin - More H2S in SkIN - & IL-22
- CAVEat mTOR? -- SNP's on CRACK - PON1 - Autism Re-ducks - Skin GAME
beYOND Gut -- MicroBEs en Masse -- Hidden Hordes --
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/f2817b80283c1f90/74a7595d664bedaf?lnk=gst&q=PMID%3A+22837109+#74a7595d664bedaf
or
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/74a7595d664bedaf

What does it mean?

Don't know..

but going to run this anyway.

So it makes me WANT to think some as we've had great gene's the
last few weeks.

Gene's for plasticity like EGR2 and FOSL2 no less.

ok

(13 hits: Thiel -- 7 hits DEGN --

http://www.eurekalert.org/pub_releases/2012-11/au-rdi110612.php
or
http://www.news-medical.net/news/20121107/MASP-1-enzyme-plays-a-central-role-in-activating-the-complement-system.aspx
MASP-1 enzyme plays a central role in activating the complement system
Published on November 7, 2012 at 1:51 AM

Researchers from Aarhus University, Denmark, have now discovered an
important mechanism behind one of our most fundamental lines of immune
function. The discovery has been published in the esteemed scientific
journal, The Journal of Immunology, where it has been highlighted as a
top story.

In collaboration with colleagues from USA and Turkey, they have
discovered exactly which enzymes collaborate in the first line of the
immune defence. Thus, they answer a central question about the so-
called complement system, which has been a focal point of the
scientific field for the past decade: which enzyme does what?

Using blood samples from a unique patient harbouring a rare genetic
syndrome, the researchers from Aarhus University have now established
that it is the enzyme MASP-1 that is key to the activation of the
complement system.

"Understanding the immune system is a central goal in itself in
scientific terms, especially for our research group conducting basic
research. But in the longer run, it is also an important goal that
this knowledge may help people and cure diseases", says postdoc Soeren
Egedal Degn from Aarhus University, who is first author on the paper.

Big perspectives for patients

He believes that once one has defined how the complement system works,
it will be possible to manipulate it:

"For example this system is important for the survival of patients
undergoing chemotherapy, because this treatment suppresses other
functions of the immune system - so in their case it is beneficial to
"rev up" the system. But following a heart attack there may be reasons
to instead dampen the system. The complement system has an unfortunate
tendency to attack tissues that have suffered damage due to
deprivation of oxygen, and thereby it exacerbates the damage already
done to the heart", says Soeren Egedal Degn.

He notes however, that the new discovery is unlikely to result in
concrete new treatment modalities in this decade.

MASP-1 and the lectin pathway

Behind the discovery of the central role of MASP-1 in the complement
system is, apart from Soeren Egedal (SE) Degn, also the Aarhus
professors Jens Chr. Jensenius and Steffen Thiel, who are considered
international experts in the field. They have previously discovered
the four other known proteins related to MASP-1, namely MASP-2,
MASP-3, MAp19 and MAp44. Together, these proteins make up a central
part of the activation pathway of complement known as the lectin
pathway. The research group in Aarhus, which also includes the
laboratory technicians Lisbeth Jensen and Annette G. Hansen, has been
central in the elucidation of the lectin pathway through the past 15
years.

The enzyme MASP-1 is able to efficiently auto-activate, for example
when it "senses" a bacterium. It then activates MASP-2, which in turn
activates the rest of the complement system in a cascade-like manner,
where a long list of enzymes sequentially activate each other - much
like dominoes. The result is a signal to immune cells to home to the
area in the body, where the system is activated, and to kill the
intruding bacteria. The bacteria are also covered in "molecular tags",
making it easier for the immune cells to recognize and efficiently
engulf them. Finally, the complement system directly "punches holes"
in the bacteria, by forming pore-like structures in their membranes.
<snip>

This work has been supported by the Lundbeck Foundation, The Novo
Nordic Foundation, as well as the Danish Council for Independent
Research - Medical Sciences. Soeren Egedal Degn is employed at the
Department of Biomedicine, Aarhus University, through a postdoctoral
fellowship from the Carlsberg Foundation.
<snip>


http://en.wikipedia.org/wiki/MASP1_(protein)
Mannan-binding lectin serine protease 1 also known as mannose-
associated serine protease 1 (MASP-1) is an enzyme that in humans is
encoded by the MASP1 gene.[1][2][3]

MASP-1 is involved in the lectin pathway of the complement system and
is responsible for cleaving C4 and C2 to form C4b2a, a C3-convertase.
[4]

MASP-1 is a serine protease that functions as a component of the
lectin pathway of complement activation. The complement pathway plays
an essential role in the innate and adaptive immune response. MASP-1
is synthesized as a zymogen and is activated when it complexes with
the pathogen recognition molecules of lectin pathway, the mannose-
binding lectin and the ficolins. This protein is not directly involved
in complement activation but may play a role as an amplifier of
complement activation by cleaving complement C2 or by activating
another complement serine protease, MASP-2. MASP-1 is also able to
cleave fibrinogen and factor XIII and may may be involved in
coagulation. A splice variant of this gene which lacks the serine
protease domain functions as an inhibitor of the complement pathway.
[3]
<snip>

http://en.wikipedia.org/wiki/Mannan-binding_lectin
Mannose-binding lectin (MBL), also called mannose-binding protein or
mannan-binding protein (MBP), is a lectin that is instrumental in
innate immunity


http://en.wikipedia.org/wiki/Mannan-binding_lectin#Function
Function

MBL belongs to the class of collectins in the C-type lectin
superfamily, whose function appears to be pattern recognition in the
first line of defense in the pre-immune host. MBL recognizes
carbohydrate patterns, found on the surface of a large number of
pathogenic micro-organisms, including bacteria, viruses, protozoa and
fungi. Binding of MBL to a micro-organism results in activation of the
lectin pathway of the complement system.

Another important function of MBL is that this molecule binds
senescent[11] and apoptotic cells and enhances engulfment of whole,
intact apoptotic cells, as well as cell debris by phagocytes.[12][13]

Activation
The complement system can be activated through three pathways the
classical pathway, the alternative pathway, and the lectin pathway.
One way that the most-recently discovered lectin pathway is activated
through the mannose-binding lectin protein. MBL binds to carbohydrates
(to be specific, mannose and fucose residues) found on the surface of
many pathogens.

For example, MBL has been show to bind to:
yeasts such as Candida albicans[14]

viruses such as HIV[15] and influenza A
many bacteria including Salmonella and Streptococci (strep/staph --
>candida et al see: xx:)


see- XX:) -
13 hits -for sallusto Staphylococcus randall zielinski- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=sallusto+Staphylococcus+randall+zielinski&start=0&
<snip>

http://en.wikipedia.org/wiki/Innate_immunity

And looking at PMID: 22966085 for SE DEGN et al....i find something
from them.. from a monthish earlier i never posted ... YET.


=====================

ok i ... i put this together on 9/18/2012 iirc.

(so some of the above may over-LAP:)

Wait a minute stupid poopid tar baby randall.

it ALL over LAPs... you moron..

whoops.. i forgot.. my blab. LOL

--------------------

http://www.nature.com/ni/journal/v13/n10/full/ni.2430.html
A balancing act

Nature Immunology 13, 901 (2012) doi:10.1038/ni.2430
Published online 18 September 2012

Basic checkpoints and redundant modulatory mechanisms allow immune
responses that are both efficient against pathogens and safe to the
host.


The traditional view of an immune system activated by foreign
molecular triggers or defined components of modified self is now
evolving into that of a system tuned to detect additional alterations
in tissue or organism homeostasis, including more elusive signals such
as changes in metabolic rate, enzymatic activity or the location of
various molecular components. Although the idea that the immune system
has evolved to maintain the homeostasis of the organism is not new,
the great variability of triggers, the versatility of the sensors and
the complex interplay between effector and regulatory networks suggest
that the ultimate function of an immune response, beyond the simple
eradication of pathogens, is to allow a return to homeostasis.
Additional complexities of the immune response, such as the interplay
between basic and specialized cellular functions, suggest a highly
balanced act that requires various checks as well as overlapping or
redundant degrees of modulation that allow efficient immune responses
with minimal collateral damage to the host.

In several specially commissioned articles, this Focus on Checks and
Balances in the Immune System

(http://www.nature.com/ni/focus/checksandbalances) explores the
cellular and molecular regulatory modules built in at every level of
the system to fine-tune the immune response and limit the amount of
tissue damage that can ensue and reviews recent progress in
understanding how basic cellular processes such as cell metabolism are
integrated into the more specialized function of immune cells to
sustain efficient responses.

In a Focus Review, Ruoning Wong and Douglas Green discuss how cell
metabolism interconnects with signaling events in cells of the immune
system to provide the energy and functional requirements of
immunological processes, such as rapid proliferation, differentiation
and functional specialization. This is explored mainly in the context
of metabolic reprogramming of T lymphocytes during activation. The
author discuss aspects of metabolic reprogramming and its consequences
in terms of 'metabolic checkpoints', which they define as molecular
mechanisms that sense metabolic status and, in turn, regulate cellular
functions. Understanding these checkpoints has become key to the study
of metabolic disorders, cancer and immune responses.

Because of the potent effector mechanisms deployed by an ongoing
immune response, the potential to induce self-damage in the host is
very high. The commissioned pieces discuss various aspects of the
balance between an effective immune response and avoiding excessive
tissue damage. Ron Germain authors a Commentary that places the
regulatory modules embedded in an immune response in the larger
context of systems organization and tackles the design principles of
such mechanisms. This provocative piece puts forward concepts such as
the fractal nature of the regulatory strategies that operate in a
cell, a tissue or an organism and touches on considerations that are
not so frequently discussed, such as the time-and-space subtleties in
which particular factors function during an immune response.

Two Reviews discuss the regulatory mechanisms that restrain signaling
though Toll-like receptors, as the main initiators of inflammation,
and outline the soluble mediators that modulate and restrain
inflammation. Peter Murray and Steve Smale define several
interconnected 'strata' that restrain inflammation, from anatomy to
the processing and secretion of proteins, and illustrate how anti-
inflammatory factors such as IL-10 function in the context of these
regulatory layers. Jacques Banchereau, Virginia Pasqual and Anne
O'Garra present an updated discussion of how cytokines modulate
inflammation in a Review that revisits the old participants IL-2,
IL-10 and TGF-β and introduces the newcomers IL-27, IL-35 and IL-37.

In the final Review of the Focus, Romina Goldszmid and Giorgio
Trinchieri present the pathogenic effects of immune responses or, as
the authors introduce it, the 'price of immunity'. Their discussion
focuses on the complex interactions between the immune response and
the microbiota and the accumulating evidence that commensals have an
active role in mucosal and skin pathologies associated with immune
responses, but it also touches on the issue of collateral tissue and
systemic damage caused by immunity to viruses and the ensuing
susceptibility to superinfections, acute immunopathology, chronic
inflammation and carcinogenesis that can be the consequence of such
responses.

This Focus attempts to provide an integrated view of the immune system
as a set of mechanisms designed to preserve the integrity of the
organism against various homeostatic disturbances. Although pathogens
represent the main source of homeostatic stress, and immune responses
engage complex cellular and molecular mediators to fight viruses and
microbes, the elimination or eradication of such pathogens may not
always be compatible with the ultimate goal, which is the preservation
of self. From this point of view, the maintenance of a suboptimal
state, such as chronic infection, that still allows survival may be
preferable to the ultimate pathogen eradication associated with
extensive damage to self. Components of the organism have evolved
various protective mechanisms against immune responses, and in most
cases the immune response itself seems to follow the path of least
harm. When these regulatory modules are lost or damaged, however,
considerable pathology ensues. Understanding the principles and
mechanisms of these regulatory modules is essential for the prevention
and treatment of disease.
<snip>


==================


Hooray for the DANEs and Hungarians!

TEAM work really wORKs!

Will it work for psoriatics with leaky guts and excess LPS?

Or is it else where we seek the truth?

-----------

http://www.biocompare.com/Life-Science-News/120834-Chain-Reaction-In-The-Human-Immune-System-Trapped-In-Crystals/
Chain Reaction In The Human Immune System Trapped In Crystals
Wednesday, September 12, 2012

Source : Aarhus University

A research team from Aarhus University has revealed details of how a
chain reaction in the human immune system starts. With these results,
the researchers hope to promote the development of strategies aimed at
alleviating suffering caused by unintentional activation of the immune
system.

The complement system is part of the innate immune system and is
composed of about 40 different proteins that work together to defend
the body against disease-causing microorganisms. The complement system
perceives danger signals in the body by recognising characteristic
molecular patterns presented by pathogenic microorganisms or some of
our own sick or dying cells that must be eliminated.

The complement system can be found in the blood, but also in the fluid
surrounding the cells in tissues. Complement serves as the first line
of defence against many pathogenic organisms, and its recognition of
danger signals is handled by specialised proteins in the complement
system.

For more than 20 years, Professor Steffen Thiel at the Department of
Biomedicine, Aarhus University, has been a world leader in studies of
MBL and MASP-2, which are two key proteins in the complement system.
When MBL recognises the danger signal, MASP-2 is converted into an
active enzyme that can now cleave the protein C4, a third important
protein in the complement system. This cleavage is the first step in a
chain reaction that ends with the elimination of pathogenic bacteria
and dying cells. A research team led by Associate Professor Gregers R.
Andersen at the Department of Molecular Biology and Genetics, Aarhus
University, has now – in collaboration with Professor Thiel –
succeeded in determining in atomic detail how the active enzyme MASP-2
recognises the substrate C4.

Crystals shot with X-rays

Two PhD students in molecular biology, Rune T. Kidmose and Nick S.
Laursen, isolated the protein C4 from blood plasma, whereas they
obtained the MASP-2 from Hungarian colleagues. They then crystallised
the substrate C4 alone, but – to their surprise – they could also
crystallise the enzyme-substrate complex C4·MASP-2. By exposing the
resulting crystals to intense X-ray radiation, the two students
managed within a year to determine the atomic structures of the C4
protein and the C4·MASP-2 complex. Two other PhD students, Sofia
Sirotkina and Troels R. Kjaer, then performed laboratory experiments
showing that the conclusions based on crystal structures were also
valid when MASP-2 cleaved C4 in a test tube.Potential impact on drug
development

The results obtained by Rune T. Kidmose and Nick S. Laursen are
remarkable. “It’s extremely rare that you can trap a proteolytic
(protein-degrading) enzyme in the middle of the process of cleaving an
intact protein,” says Associate Professor Gregers Rom Andersen, the
students’ supervisor. “We now know in detail which parts of MASP-2
recognise the substrate C4. Another fascinating aspect of their
results is that we also know the structure of both C4 and MASP-2
alone, so we can see how both the enzyme and the substrate change
their three-dimensional structure when C4 is recognised by MASP-2. We
can also see how these changes directly contribute to facilitating the
cleavage of C4,” he concludes.

For Professor Thiel, the new results represent a completely new way to
visualise how MASP-2 – whose function he discovered in 1997 – carries
out its function. “It’s also a great personal pleasure to be involved
right from the discovery of a new protein to the point where you
obtain knowledge at the atomic level on how this protein functions as
an enzyme,” he says.

In many situations, an undesirable activation of the complement system
takes place, which can damage our own tissues. Several pharmaceutical
companies are currently working on developing drugs that can attenuate
such damage. “The very detailed understanding that we now have
concerning parts of the complement system will undoubtedly lead to
more intelligent ways of developing new drugs,” says Professor Thiel.
“Of course, we won’t stop our studies here, as we’ll continue the very
detailed studies of other proteins and molecular mechanisms within the
immune system,” he continues.

The new results from Aarhus University have just been published in the
prestigious journal Proceedings of the National Academy of Sciences
(PNAS).
<snip>


http://www.ncbi.nlm.nih.gov/pubmed/22949645
Proc Natl Acad Sci U S A. 2012 Sep 4.
Structural basis for activation of the complement system by component
C4 cleavage

Kidmose RT, Laursen NS, Dobó J, Kjaer TR, Sirotkina S, Yatime L,
Sottrup-Jensen L, __Thiel S__, Gál P, Andersen GR.

Source
Departments of Molecular Biology and Genetics and Biomedicine, Aarhus
University, DK-8000 Aarhus, Denmark.

Abstract
An essential aspect of innate immunity is recognition of molecular
patterns on the surface of pathogens or altered self through the
lectin and classical pathways, two of the three well-established
activation pathways of the complement system. This recognition causes
activation of the MASP-2 or the C1s serine proteases followed by
cleavage of the protein C4. Here we present the crystal structures of
the 203-kDa human C4 and the 245-kDa C4⋅MASP-2 substrate⋅enzyme
complex. When C4 binds to MASP-2, substantial conformational changes
in C4 are induced, and its scissile bond region becomes ordered and
inserted into the protease catalytic site in a manner canonical to
serine proteases. In MASP-2, an exosite located within the CCP domains
recognizes the C4 C345C domain 60 Å from the scissile bond. Mutations
in C4 and MASP-2 residues at the C345C-CCP interface inhibit the
intermolecular interaction and C4 cleavage. The possible assembly of
the huge in vivo enzyme-substrate complex consisting of glycan-bound
mannan-binding lectin, MASP-2, and C4 is discussed. Our own and prior
functional data suggest that C1s in the classical pathway of
complement activated by, e.g., antigen-antibody complexes, also
recognizes the C4 C345C domain through a CCP exosite. Our results
provide a unified structural framework for understanding the early and
essential step of C4 cleavage in the elimination of pathogens and
altered self through two major pathways of complement activation.

PMID: 22949645

Steffen Thiel - 276 hits:
http://www.ncbi.nlm.nih.gov/pubmed?term=Thiel%20S%5BAuthor%5D

And PMID: 22949645 is #2 of 276

---------------

11 hits: complement + C4 - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=complement+c4&start=0&

237 hits: complement -- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=complement&start=0&scoring=d&
by relevance
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=complement&start=0&


30 of 237 have: lectin - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=complement+lectin&start=0&scoring=d&

Two hits with: masp lectin and YKW: p ng
https://groups.google.com/groups/search?qt_s=1&q=randall+lectin+masp-2

282 hits: masp + complement -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=masp%20complement


----------

http://en.wikipedia.org/wiki/Complement_system
The complement system helps or “complements” the ability of antibodies
and phagocytic cells to clear pathogens from an organism. It is part
of the immune system called the innate immune system that is not
adaptable and does not change over the course of an individual's
lifetime. However, it can be recruited and brought into action by the
adaptive immune system.

The complement system consists of a number of small proteins found in
the blood, generally synthesized by the liver, and normally
circulating as inactive precursors (pro-proteins). When stimulated by
one of several triggers, proteases in the system cleave specific
proteins to release cytokines and initiate an amplifying cascade of
further cleavages. The end-result of this activation cascade is
massive amplification of the response and activation of the cell-
killing membrane attack complex. Over 25 proteins and protein
fragments make up the complement system, including serum proteins,
serosal proteins, and cell membrane receptors. They account for about
5% of the globulin fraction of blood serum.

Three biochemical pathways activate the complement system: the
classical complement pathway, the alternative complement pathway, and
the lectin pathway.[1]
<snip>

http://en.wikipedia.org/wiki/Lectin_pathway

[...] MBL
MBL is a 6- to 18-headed molecule that forms a complex with MASP-1
(Mananose-binding lectin-Associated Serine Protease), MASP-2 and
MASP-3, that are protease zymogens. The MASPs are very similar to C1r
and C1s molecules of the classical complement pathway, respectively,
and are thought to have a common evolutionary ancestor. When the
carbohydrate-recognising heads of MBL bind to specifically arranged
mannose residues on the surface of a pathogen, MASP-1 and MASP-2 are
activated to cleave complement components C4 and C2 into C4a, C4b,
C2a, and C2b. In addition, two smaller MBL-associated proteins (MAps)
are found in complex with MBL. MBL-associated protein of 19 kDa
(MAp19) and MBL-associated protein of 44 kDa (Map44). MASP-1, MASP-3
and MAp44 are alternative splice products of the MASP1 gene, while
MASP-2 and MAp19 are alternative splice products of the MASP-2 gene.
MAp44 has been suggested to act as a competitive inhibitor of lectin
pathway activation, by displacing MASP-2 from MBL, hence preventing
cleavage of C4 and C2 [2]

[...] Clinical significance

It has been found that people deficient in MBL experience a
substantial increase in infections during the early years of
childhood.
<snip>

http://en.wikipedia.org/wiki/Map44
Mannose-binding lectin-associated protein of 44 kDa (MAp44) is a
protein arising from the human MASP1 gene. MASP-1, MASP-3 and MAp44
are alternative splice products of the MASP1 gene. MAp44 has been
suggested to act as a competitive inhibitor of lectin pathway
activation, by displacing MASP-2 from MBL, hence preventing cleavage
of C4 and C2 [1]
<snip>

http://en.wikipedia.org/wiki/Complement_component_4



^^^^^^^^^^^^^^^^^^^^^^

#1 of 276 for steffen Thiel:

and 144 of 276 for thiel has: complement
http://www.ncbi.nlm.nih.gov/pubmed?term=Thiel%20S%5BAuthor%5D%20complement

#1 of 144 and 276:

http://www.ncbi.nlm.nih.gov/pubmed/22966085
J Immunol. 2012 Sep 10.
Mannan-Binding Lectin-Associated Serine Protease (MASP)-1 Is Crucial
for Lectin Pathway Activation in Human Serum, whereas neither MASP-1
nor MASP-3 Is Required for Alternative Pathway Function.

Degn SE, Jensen L, Hansen AG, Duman D, Tekin M, Jensenius JC, Thiel S.

Source
Department of Biomedicine, Aarhus University, DK-8000 Aarhus C,
Denmark;

Abstract
The lectin pathway of complement is an important component of innate
immunity. Its activation has been thought to occur via recognition of
pathogens by mannan-binding lectin (MBL) or ficolins in complex with
MBL-associated serine protease (MASP)-2, followed by MASP-2
autoactivation and cleavage of C4 and C2 generating the C3 convertase.
MASP-1 and MASP-3 are related proteases found in similar complexes.
MASP-1 has been shown to aid MASP-2 convertase generation by auxiliary
C2 cleavage. In mice, MASP-1 and MASP-3 have been reported to be
central also to alternative pathway function through activation of
profactor D and factor B. In this study, we present functional studies
based on a patient harboring a nonsense mutation in the common part of
the MASP1 gene and hence deficient in both MASP-1 and MASP-3.
Surprisingly, we find that the alternative pathway in this patient
functions normally, and is unaffected by reconstitution with MASP-1
and MASP-3. Conversely, we find that the patient has a nonfunctional
lectin pathway, which can be restored by MASP-1, implying that this
component is crucial for complement activation. We show that, although
MASP-2 is able to autoactivate under artificial conditions, MASP-1
dramatically increases lectin pathway activity at physiological
conditions through direct activation of MASP-2. We further demonstrate
that MASP-1 and MASP-2 can associate in the same MBL complex, and that
such cocomplexes are found in serum, providing a scenario for
transactivation of MASP-2. Hence, in functional terms, it appears that
MASP-1 and MASP-2 act in a manner analogous to that of C1r and C1s of
the classical pathway.

PMID: 22966085


zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz


But is this ALL for Naught?


http://www.ncbi.nlm.nih.gov/pubmed/15948998
Br J Dermatol. 2005 Jun;152(6):1313-5.
Functional MASP2 single nucleotide polymorphism plays no role in
psoriasis.

Stover C, Barrett S, Lynch NJ, Barker JN, Burden D, Trembath R,
Schwaeble W, Veal C.

Source
Department Infection, Immunity and Inflammation, University of
Leicester, Leicester LE1 9HN, UK. cm...@le.ac.uk

Abstract
BACKGROUND:
Psoriasis is a heritable disease and genome-wide scans have implicated
several loci of susceptibility. The gene for MASP-2, a protease
involved in complement activation, is located within one of these loci
on chromosome 1p.

OBJECTIVES:
To assess whether partial or total MASP-2 deficiency is a risk factor
for developing psoriasis.

METHODS:
We screened a cohort of patients affected by plaque psoriasis and
their parents by restriction fragment length polymorphism analyses.

RESULTS:
We detected a single nucleotide polymorphism that leads to an amino
acid exchange, which results in dissociation of MASP-2 from a
carbohydrate recognition complex.

CONCLUSIONS:
We show that this mutant allele is not associated with psoriasis.
There was no favoured transmission from parents to affected offspring.
The calculated allele frequency in this psoriasis group (Scottish and
English) was 0.0326, and in the unaffected group 0.0379.

PMID: 15948998


--------------------------

344 hits: psoria* + complement -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20complement

And #1 of 344 is similar to pmid: 15948998


http://www.ncbi.nlm.nih.gov/pubmed/22837109
Hum Mutat. 2012 Jul 26. doi: 10.1002/humu.22172.
Correlating multiallelic copy number polymorphisms with disease
susceptibility.

Cantsilieris S, White SJ.

Source
Centre for Reproduction and Development, Monash Institute of Medical
Research, Monash University, Melbourne, Victoria, Australia; Centre
for Eye Research Australia, University of Melbourne, Royal Victorian
Eye and Ear Hospital, East Melbourne, Victoria, Australia.

Abstract
The human genome contains a significant amount of sequence variation,
from single nucleotide polymorphisms to large stretches of DNA that
may be present in a range of different copies between individuals.
Several such regions are variable in >1% of the population (referred
to as copy number polymorphisms or CNPs), and many studies have looked
for associations between the copy number of genes within multiallelic
CNPs and disease susceptibility. Associations have indeed been
described for several genes, including the β-defensins (DEFB4,
DEFB103, DEFB104), chemokine ligand 3 like 1 (CCL3L1), Fc gamma
receptor 3B (FCGR3B), and complement component C4 (C4). However,
follow-up replication in independent cohorts has failed to reproduce a
number of these associations. It is clear that replicated associations
such as those between C4 and systemic lupus erythematosus, and β-
defensin and psoriasis, have used robust genotyping methodologies.
Technical issues associated with genotyping sequences of high identity
may therefore account for failure to replicate other associations.
Here, we compare and contrast the most popular approaches that have
been used to genotype CNPs, describe how they have been applied in
different situations, and discuss potential reasons for the difficulty
in reproducibly linking multiallelic CNPs to complex diseases.

PMID: 22837109

So we go to selectin's?

102 hits: selectin's - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=selectin%27s&start=0&scoring=d&


with 146 hits: selectin + psoria* - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20selectin


#1 of 146


http://www.ncbi.nlm.nih.gov/pubmed/22882471
J Eur Acad Dermatol Venereol. 2012 Aug 7. doi: 10.1111/j.
1468-3083.2012.04671.x.
Increased number of circulating endothelial cells (CECs) in patients
with psoriasis - preliminary report.

Batycka-Baran A, Paprocka M, Krawczenko A, Duś D, Szepietowski JC.

Source
Department of Dermatology, Venereology and Allergology Wroclaw Medical
University, Chalubinskiego, Wroclaw, Poland Institute of Immunology
and Experimental Therapy, Polish Academy of Sciences, Rudolfa Weigla,
Wroclaw, Poland.

Abstract
Background  Numerous studies have demonstrated increased
cardiovascular risk in psoriasis. Circulating endothelial cells (CECs)
have been proposed as a new marker of endothelial dysfunction that
plays an important role in pathogenesis of atherosclerosis. Objective
The aim of this study was to compare the number of CECs in psoriatic
patients to a control group and to analyze possible correlations
between the numbers of CECs and the plasma levels of classical markers
of endothelial dysfunction, such as: sICAM-1, sE-selectin and von
Willebrand factor (vWF). Methods  The number of CECs, identified as
CD146 + / CD45- cells, were determined in peripheral blood with using
flow cytometry in psoriatic patients (n = 63) and controls (n = 31).
The plasma levels of: sICAM-1, sE-selectin, vWF were measured with
ELISA. The severity of psoriasis was assessed with PASI. Results  The
number of CECs was significantly increased in psoriatic patients
compared with controls (P < 0.00001) and positively correlated with
disease severity (R = 0.360; P = 0.0037). The levels of sICAM-1, sE-
selectin and vWF were significantly elevated in psoriatic patients (P
< 0.00001; P < 0.00001; P = 0.00072, respectively). The number of CECs
was significantly, positively correlated with the levels of sICAM-1 (R
= 0.393; P = 0.0014) and vWF (R = 0.314; P = 0.012) in psoriatic
patients. The levels of sICAM-1 and sE-selectin were positively
correlated with disease severity (R = 0.356; P = 0.0041 and R = 0.407;
P = 0.0009, respectively). Conclusion  The increased number of CECs
that correlates with disease severity and plasma levels of sICAM-1 and
vWF may indicate endothelial dysfunction or injury in patients with
psoriasis.

PMID: 22882471


Yet could card14 mutation account for the above paucity of selectins
by increased inflammation?


I don't KNOW but suspect so.


So we go back to bungle in the jungle?

It does work... you know?

That fern kalawalla does.

And now this oleorsin.


59 hits: psoria* + LPS -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20lps


#1 of 59:


http://www.ncbi.nlm.nih.gov/pubmed/22939967
Int J Pharm. 2012 Aug 20.
GC-MS profiling of the phytochemical constituents of the oleoresin
from Copaifera langsdorffii Desf. and a preliminary in vivo evaluation
of its antipsoriatic effect.

Gelmini F, Beretta G, Anselmi C, Centini M, Magni P, Ruscica M,
Cavalchini A, Maffei Facino R.

Source
Department of Pharmaceutical Sciences, University of Milan, Via
Mangiagalli 25, 20133 Milan, Italy.

Abstract
Copaiba is the oleoresin (OR) obtained from Copaifera (Fabaceae), a
neotropical tree which grows in Amazon regions. The balsam,
constituted by an essential oil and a resinous fraction is used as
folkloristic remedy in the treatment of several inflammatory diseases
and for its antioxidant and antibacterial properties. Aim of this work
was (a) to carry out a characterization by GC-MS of the volatile and
nonvolatile constituents of Copaifera langsdorffii Desf. oleoresin
(OR); (b) to investigate the mechanism of its anti-inflammatory
activity; (c) to evaluate its antipsoriatic effect after oral intake/
topical application. The volatile fraction (yield: 22.51%, w/w) shows:
α-bergamotene (48.38%), α-himachalene (11.17%), β-selinene (5.00%) and
β-caryophyllene (5.47%). The OR residue (77.49%, w/w), after
derivatization, showed as main constituents the following compounds:
copalic, abietic, daniellic, lambertinic, labd-7-en-15-oic, pimaric,
isopimaric acids and kaur16-en18-oic acid. Preincubation of LPS-
stimulated human THP-1 monocytes with increasing concentrations of the
OR purified fraction (OR-PF), containing diterpene acids, diterpenes
and sesquiterpenes, reduced the release of pro-inflammatory cytokines
(IL-1β, IL-6, TNFα) in a dose-range of 0.1-10μM. In addition, in cell
culture system of human THP-1 monocytes, 1μM OR-PF counteracts LPS-
driven NF-κB nuclear translocation. In a preliminary clinical trial
three patients affected by chronic psoriasis, treated with oral intake
or topical application of the OR, exhibited a significant improvement
of the typical signs of this disease, i.e. erythema, skin thickness,
and scaliness. In conclusion, the results of this work, beside an
extensive analytical characterization of the OR chemical composition,
provide strong evidences that its anti-inflammatory activity is
related to the inhibition of the NF-κB nuclear translocation, and
consequently of proinflammatory cytokines secretion.

PMID: 22939967


47 hits : complement C4 + psoria* -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=complement%20c4%20lps

11 of 47 have: lectin
http://www.ncbi.nlm.nih.gov/pubmed?term=complement%20c4%20lps%20lectin


No hits with selectin and the above.

odd or is it a cancer deal and not autoimmune?

http://en.wikipedia.org/wiki/Sialic_acid#Function
Sialic acid-rich glycoproteins (sialoglycoproteins) bind selectin in
humans and other organisms. Metastatic cancer cells often express a
high density of sialic acid-rich glycoproteins. This overexpression of
sialic acid on surfaces creates a negative charge on cell membranes.
This creates repulsion between cells (cell opposition)[4] and helps
these late-stage cancer cells enter the blood stream.

[...] Sialic acid can "hide" mannose antigens on the surface of host
cells or bacteria from mannose-binding lectin.[citation needed] This
prevents activation of complement.
<snip>


===================

one more from THIEL and SE DEGN (#2 of 12 for dEGN) et al:

http://www.ncbi.nlm.nih.gov/pubmed/22670777
Clin Exp Immunol. 2012 Jul;169(1):38-48. doi: 10.1111/j.
1365-2249.2012.04584.x.
Mannan-binding lectin (MBL)-associated serine protease-1 (MASP-1), a
serine protease associated with humoral pattern-recognition molecules:
normal and acute-phase levels in serum and stoichiometry of lectin
pathway components.

Thiel S, Jensen L, Degn SE, Nielsen HJ, Gál P, Dobó J, Jensenius JC.

Source
Department of Biomedicine, Aarhus University, Denmark.
s...@microbiology.au.dk

Abstract
The pattern-recognition molecules mannan-binding lectin (MBL) and the
three ficolins circulate in blood in complexes with MBL-associated
serine proteases (MASPs). When MBL or ficolin recognizes a
microorganism, activation of the MASPs occurs leading to activation of
the complement system, an important component of the innate immune
system. Three proteins are produced from the MASP1 gene: MASP-1 and
MASP-3 and MAp44. We present an assay specific for MASP-1, which is
based on inhibition of the binding of anti-MASP-1-specific antibody to
MASP-1 domains coated onto microtitre wells. MASP-1 was found in serum
in large complexes eluting in a position corresponding to ∼600 kDa
after gel permeation chromatography in calcium-containing buffer and
as monomers of ∼75 kDa in dissociating buffer. The concentration of
MASP-1 in donor sera (n = 105) was distributed log-normally with a
median value of 11 µg/ml (range 4-30 µg/ml). Serum and citrate plasma
levels were similar, while the values in ethylenediamine tetraacetic
acid plasma were slightly lower and in heparin plasma were 1·5 times
higher than in serum. MASP-1 was present at adult level at 1 year of
age, while it was 60% at birth. In normal healthy individuals the
level of MASP-1 was stable throughout a 2-month period. After
induction of an acute-phase reaction by operation we found an initial
short decrease, concomitant with an increase in C-reactive protein
levels, followed by an increase, doubling the MASP-1 concentration
after 2 days. The present data prepare the ground for studies on the
associations of MASP-1 levels with disease.

PMID: 22670777
PMCID: PMC3390472 [Available on 2013/7/1]


#3 of 12 for DEGN

I lied... two more instead of one as this one's got map19


http://www.ncbi.nlm.nih.gov/pubmed/21871896
J Immunol Methods. 2011 Oct 28;373(1-2):89-101. Epub 2011 Aug 17.
MAp19, the alternative splice product of the MASP2 gene.

Degn SE, Thiel S, Nielsen O, Hansen AG, Steffensen R, Jensenius JC.

Source
Department of Biomedicine, Aarhus University, Wilhelm Meyers Allé 4,
DK-8000 Aarhus C, Denmark. sd...@microbiology.au.dk

Abstract
The lectin pathway of complement is a central part of innate immunity,
but as a powerful inducer of inflammation it needs to be tightly
controlled. The MASP2 gene encodes two proteins, MASP-2 and MAp19.
MASP-2 is the serine protease responsible for lectin pathway
activation. The smaller alternative splice product, MAp19, lacks a
catalytic domain but retains two of three domains involved in
association with the pattern-recognition molecules (PRMs): mannan-
binding lectin (MBL), H-ficolin, L-ficolin and M-ficolin. MAp19
reportedly acts as a competitive inhibitor of MASP-2-mediated
complement activation. In light of a ten times lower affinity of
MAp19, versus MASP-2, for association with the PRMs, much higher serum
concentrations of MAp19 than MASP-2 would be required for MAp19 to
exert such an inhibitory activity. Just four amino acid residues
distinguish MAp19 from MASP-2, and these are conserved between man,
mouse and rat. Nonetheless we generated monoclonal rat anti-MAp19
antibodies and established a quantitative assay. We found the
concentration of MAp19 in serum to be 217 ng/ml, i.e., 11nM,
comparable to the 7 nM of MASP-2. In serum all MASP-2, but only a
minor fraction of MAp19, was associated with PRMs. In contrast to
previous reports we found that MAp19 could not compete with MASP-2 for
binding to MBL, nor could it inhibit MASP-2-mediated complement
activation. Immunohistochemical analyses combined with qRT-PCR
revealed that both MAp19 and MASP-2 were mainly expressed in
hepatocytes. High levels of MAp19 were found in urine, where MASP-2
was absent.

PMID: 21871896

8 of DEGN se--> 12 total hits has Thiel:
12 hits
http://www.ncbi.nlm.nih.gov/pubmed?term=Degn%20SE%5BAuthor%5D
8 with Degn and Thiel:
http://www.ncbi.nlm.nih.gov/pubmed?term=Degn%20SE%5BAuthor%5D%20Thiel

OTOH how much do we care beyond knowing autoimmunity?

such as
http://www.ncbi.nlm.nih.gov/pubmed/15948998
Functional MASP2 single nucleotide polymorphism plays no role in
psoriasis.
[...] PMID: 15948998

But this was 2005 so give them a BREAK already..<w>

And let's expand the masp to masp*

and we get this:


PMID: 20363977 - 3 hits on the p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+20363977+&start=0&scoring=d&

http://www.ncbi.nlm.nih.gov/pubmed/20363977
J Immunol. 2010 May 1;184(9):5392-402. Epub 2010 Apr 2.
Ezrin, maspin, peroxiredoxin 2, and heat shock protein 27: potential
targets of a streptococcal-induced autoimmune response in psoriasis.

Besgen P, Trommler P, Vollmer S, Prinz JC.

Source
Department of Dermatology, Ludwig-Maximilians-University of Munich,
Munich, Germany.

Abstract
Psoriasis is an HLA-Cw6-associated T cell-mediated autoimmune disease
of the skin that is often triggered by streptococcal angina. To
identify keratinocyte proteins, which may become psoriatic
autoantigens as the result of an immune response against streptococci,
rabbits were immunized with heat-killed Streptococcus pyogenes.
Streptococcal immunization induced Ab formation against various human
keratinocyte proteins. Sera from psoriasis patients reacted against
several of these proteins as well. Common serologic reactivities of
rabbits and patients included the proteins ezrin, maspin,
peroxiredoxin 2 (PRDX2), heat shock protein (hsp)27, and keratin 6.
When used for stimulation of blood lymphocytes, ezrin, maspin, PRDX2,
and hsp27 induced increased T cell activation in psoriasis patients,
which was particularly evident for HLA-Cw6(+) individuals. Ag-specific
T cell lines generated with these proteins consisted predominantly of
CD8(+) T cells and used TCR beta-chain rearrangements, which were
highly homologous to those expanded within the corresponding skin
lesion. Several immunodominant epitopes on the different proteins
could be defined according to sequence alignments with the whole
genome of S. pyogenes. Our data indicate that maspin, ezrin, PRDX2,
hsp27, and potentially keratin 6 could act as autoantigens of a
streptococcal-induced autoimmune response and represent targets of the
exaggerated T cell response in psoriasis. Additionally, ezrin and
hsp27 might constitute antigenic links between psoriasis and
inflammatory bowel disease, uveitis, or arteriosclerosis, which are
clinically associated.

PMID: 20363977
Free full text

But maspin is in serpin family so no go...
http://en.wikipedia.org/wiki/Maspin

Maybe maspin and masp have some tricks betwixt but not for here and
now goys.


^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^

As to maspin and NO.. i've posted this next abstract 3 times..

what does that mean?

I'm still wondering? LOL


J Immunol. 2010 May 1;184(9):5392-402. Epub 2010 Apr 2.
Ezrin, maspin, peroxiredoxin 2, and heat shock protein 27: potential
targets of a streptococcal-induced autoimmune response in psoriasis.
Besgen P, Trommler P, Vollmer S, Prinz JC.
Source
Department of Dermatology, Ludwig-Maximilians-University of Munich,
Munich, Germany.
Abstract
Psoriasis is an HLA-Cw6-associated T cell-mediated autoimmune disease
of the skin that is often triggered by streptococcal angina. To
identify keratinocyte proteins, which may become psoriatic
autoantigens as the result of an immune response against streptococci,
rabbits were immunized with heat-killed Streptococcus pyogenes.
Streptococcal immunization induced Ab formation against various human
keratinocyte proteins. Sera frompsoriasis patients reacted against
several of these proteins as well. Common serologic reactivities of
rabbits and patients included the proteins ezrin,maspin, peroxiredoxin
2 (PRDX2), heat shock protein (hsp)27, and keratin 6. When used for
stimulation of blood lymphocytes, ezrin, maspin, PRDX2, and hsp27
induced increased T cell activation in psoriasis patients, which was
particularly evident for HLA-Cw6(+) individuals. Ag-specific T cell
lines generated with these proteins consisted predominantly of CD8(+)
T cells and used TCR beta-chain rearrangements, which were highly
homologous to those expanded within the corresponding skin lesion.
Several immunodominant epitopes on the different proteins could be
defined according to sequence alignments with the whole genome of S.
pyogenes. Our data indicate that maspin, ezrin, PRDX2, hsp27, and
potentially keratin 6 could act as autoantigens of a streptococcal-
induced autoimmune response and represent targets of the exaggerated T
cell response in psoriasis. Additionally, ezrin and hsp27 might
constitute antigenic links between psoriasis and inflammatory bowel
disease, uveitis, or arteriosclerosis, which are clinically
associated.

PMID: 20363977
Free full text


hence:
10 hits : maspin + nitric oxide - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=maspin%20nitric%20oxide

And we all go back to cruier and NO and how did he knock his psoriasis
down in record time that one time he can't duplicate NOW. LOL


OK... will do some egr2 and FOSL2 today if i get my head around it.


randall.. OH.. and happy FECAL Cliff day! Dont' drive drunk.. i hate
that!