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Diet Psor & Diet -- two point OH? - Trigger - Onset -Pustular (PPP) & Th17 -->SFB-->RAMifications _ HONDA - Littman & Ivanov -->Clostridium (CANCER time?)-->TREGs-- >L. Plantarum! :O more!
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randall
Dec 7, 2012, 5:10:05 PM12/7/12
to
hey
NOT for BB if he can choose to NOT OPEN this.
Not sure how BB Does that but i've stopped posting so we can work it
OUT. :)
And thus i start a new thread:
The old thread:
link:
Thurs, Dec 6 2012 6:42 pm
Subject: Re: A dietary psoriasis treatment
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/204a20b22275d0e1
you said in the ABOVE thread:
------------
FromTheRafters
View profile
More options Dec 6, 6:42 pm
JRStern used his keyboard to write :
- Hide quoted text -
> On Wed, 05 Dec 2012 20:11:54 -0500, FromTheRafters
> <erra...@nomail.afraid.org> wrote:
>> JRStern wrote :
>>> On Mon, 3 Dec 2012 23:23:02 -0800 (PST), randall <ranhu...@aol.com>
>>> wrote:
>>>> OK, so what tips the SCALEs for you, more then say curcumin?
>>> My curcumin cocktail with fish oil and vitamin C, and now with black
>>> pepper, plus mass quantities of Curel, and also now using Dove
>>> moisturizing body wash instead of previous more harsh soaps. I'm not
>>> clear, nothing has cleared me since I got this thing, but this
>>> regimen, and long-sleeve shirts, keep me up and moving about in the
>>> world.
>> How long has this flare-up lasted, if you don't mind my asking? Also,
>> if you've had more than one flare-up - how long was the remission
>> period?
>> [...]
> Never had a clearing in 20+ years.
> Not what I wanted to hear, I'm newly diagnosed and still have hopes of
> lengthy remission.
> Within the chronic condition I've had flare-ups that slowly trained me
> as to ways to avoid them and guided me towards better maintenance
> strategies.
Hopefully I can get to recognize my triggers and learn to avoid them
too. For now it's visits to the easy-bake oven and smearing
clobetasol
on the affected areas. I really don't want pills or shots, but it may
come to that.
Thanks for replying, I wasn't sure if my choice of NNTP server was
blocked in this group.
---------------------------
Thus:
Does this help BB to figure out HOW not to OPEN my THREADS?
I will start my OWN group and then use links to THESE LONG posts chock
a block
full of pubmed ABSTRACTS....
Which... IMO... science DOES matter... (<G><w>)
http://en.wikipedia.org/wiki/NNTP
http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
And will bohgosity cop to which of these he's using?
http://en.wikipedia.org/wiki/Comparison_of_Usenet_newsreaders
So we know how this works?
Maybe FromtheRAFTERs can tell us or me?
and RAFTER and his PPP
If/When you onset with pustular there had to BE a Trigger.
Or so we've been led to believe.
So once it happens an epicgenetic event onsets that doesn't change in
the course of having psoriasis almost 100% of the time..
Unless you use TNF blocker's till the day you expire..
The trigger:
Something like antibiotics or STREP (candida et al) for instance.
Noticed - rafter --> ppp- link:
http://www.everydayhealth.com/psoriasis/living-with-pustular-psoriasis.aspx
If it had been hpa-axis susan the game would be a FOOT. LoL
Elementary as i'm watching it.. LOL
<I was doing this last night while enjoying sherlock "elementary" and
cute watson [ lucy Liu])
http://www.huffingtonpost.com/2012/09/27/elementary-lucy-liu_n_1919614.html
ok enough of that segue..but but but...
yes id squid?
Well doesn't her left eye look oriental and her RIGHT eye look
westernized if there
be such a non symmetrical thingy pooh?
I don't know id squid.. good question.. will think it over and OUT..
LOL
----------------
ok..carry on tar baby..
Does affected skin look like this:
http://upload.wikimedia.org/wikipedia/en/9/91/Acute_generalized_exanthematous_pustulosis.jpg
http://en.wikipedia.org/wiki/Acute_generalized_exanthematous_pustulosis
Acute generalized exanthematous pustulosis (AGEP) (also known as
"Pustular drug eruption," and "Toxic pustuloderma") is a not uncommon
cutaneous reaction pattern that in 90% of cases is related to
medication administration, characterized by a sudden eruption that
appears on average five days after the medication is started.[1]:124
It is mediated by T cells.[2]
Presentation
AGEP is an acute febrile drug eruption characterized by numerous
small, primarily non-follicular, sterile pustules, arising within
large areas of edematous erythema.[3]
The eruption follows a self-limiting course and will end before a week
provided the causative agent (e.g. medication) is discarded. It is
accompanied by fever, neutrophilia, and sometimes by facial edema,
hepatitis and eosinophilia. The mortality rate is about 5% and the
differential diagnosis includes Stevens–Johnson syndrome (SJS).
Contrary to SJS, in AGEP, mucosa are not affected, which means that
there are no blisters in the mouth or vagina.
Treatment
The treatment is (1) stop the offending drug (antibiotics), (2)
symptomatic (fever) and (3) for complications (hepatitis).[4]
<snip>
ppp
http://en.wikipedia.org/wiki/Pustulosis
Pustulosis is highly inflammatory skin condition resulting in large
fluid-filled blister-like areas - pustules. Pustulosis typically
occurs on the palms of the hands and/or the soles of the feet. The
skin of these areas peels and flakes (exfoliates).[1] This condition-
also referred to as "palmo-plantar pustulosis" - is a feature of
pustular psoriasis.
Pustular - 1,080 hits- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=+pustular&start=0&
ppp - 145 hits - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=ppp&start=0&
palmoplantar pustular psoriasis - 17 hit -p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=palmoplantar+pustular+psoriasis&start=0&
1340 all groups
https://groups.google.com/groups/search?qt_s=1&q=palmoplantar+pustular+psoriasis
http://en.wikipedia.org/wiki/Pustulosis_palmaris_et_plantaris
Pustulosis palmaris et plantaris (also known as "Pustulosis of palms
and soles,"[1] "Palmoplantar pustulosis," "Persistent palmoplantar
pustulosis," "Pustular psoriasis of the Barber type," and "Pustular
psoriasis of the extremities") is a chronic recurrent pustular
dermatosis localized on the palms and soles only, characterized
histologically by intraepidermal vesicles filled with neutrophils.[2]:
411,628[3]:204
<snip>
1091 hits - psoria* + pustular - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20pustular
http://www.ncbi.nlm.nih.gov/pubmed/22426986
Serum and tissue levels of IL-17 in different clinical subtypes of
psoriasis.
Yilmaz SB, Cicek N, Coskun M, Yegin O, Alpsoy E.
Source
Department of Dermatology and Venereology, Akdeniz University School
of Medicine, Antalya, Turkey.
Abstract
Serum IL-17 levels and IL-17 mRNA expression have been reported to be
higher in psoriatic skin than normal skin. There are very limited data
in the literature about difference in the levels of this cytokine in
various clinical disease subtypes. We aimed to evaluate whether there
is a difference in the level of this cytokine according to clinical
subtypes of psoriasis. 70 psoriasis patients (30 plaque psoriasis, 20
guttate psoriasis, and 20 pustular psoriasis) and 50 age- and sex-
matched healthy volunteers were included in the study. Serum IL-17
levels were determined by ELISA. Skin biopsies obtained from lesions
and non-lesional skin area of 12 patients and healthy individuals (n =
5) were analyzed by quantitative PCR (qPCR) to measure the mRNA levels
of IL-17. Statistically, the serum IL-17 levels did not exhibit any
difference between the patients and control groups. However, analysis
of each subgroup revealed that the IL-17 levels were significantly
higher in pustular psoriasis group (10.09 ± 12.6 pg/ml) than controls
(4.4 ± 4.1 pg/ml) (p = 0.02). In addition, the IL-17 levels of plaque
psoriasis patients with PASI score ≥10 (11.30 ± 6.0 pg/ml) were
significantly higher than that of patients with PASI score <10 (3.39 ±
2.6 pg/ml) and controls (p < 0.001). The Pearson correlation analysis
showed a positive correlation between the serum IL-17 levels and PASI.
Lesional skin samples of psoriasis patients showed significantly
higher levels of IL-17 mRNA compared with perilesional skin samples (p
= 0.017). Also, in the pustular psoriasis, IL-17 mRNA levels were
found to be distinctively high in comparison with other clinical
subtypes and healthy controls. Our results indicate that IL-17 and
Th17 cells have an important role in pustular psoriasis and severe
psoriasis.
PMID: 22426986
And a heart FELT cardio delight:
http://www.ncbi.nlm.nih.gov/pubmed/19661531
J Rheumatol Suppl. 2009 Aug;83:19-20.
Clinical aspects and comorbidities of psoriasis.
Ayala F, Ayala F.
Source
Division of Dermatology, Department of Systematic Pathology,
University of Naples Federico II, I 80131 Naples, Italy.
Abstract
Psoriasis is a disease mediated by Th1 and Th17 cytokines that has
different phenotypes (plaque, guttate, pustular, and erythrodermic
type). Aside from the well known psoriatic arthritis, associated
disorders may occur more frequently than expected, including Crohn's
disease, anxiety/depression, and metabolic syndrome. This is based on
a constellation of different factors, including abdominal obesity,
atherogenic dyslipidemia, hypertension, and glucose intolerance, and
is a strong predictor of type 2 diabetes, cardiovascular disease, and
stroke. People with moderate to severe psoriasis have more risk for
cardiac disease, presumably due to the inflammatory nature of
psoriasis, causing inflammatory changes in coronary arteries. The
strong association between psoriasis and obesity potentially makes
psoriasis an important healthcare issue. Since cardiovascular risk
factors are higher in psoriatic patients, dermatologists treating
moderate to severe psoriasis should screen for their presence, thus
approaching psoriasis as a potential multisystem disorder.
PMID: 19661531
And since this next one has a full text i'm having a little FUN.
now
http://www.ncbi.nlm.nih.gov/pubmed/19059833
Eur J Dermatol. 2009 Jan-Feb;19(1):69-71. Epub 2008 Dec 5.
Bullous pemphigoid followed by pustular psoriasis showing Th1, Th2,
Treg and Th17 immunological changes.
Yasukawa S, Dainichi T, Kokuba H, Moroi Y, Urabe K, Hashimoto T, Furue
M.
Source
Department of Dermatology, Graduate School of Medical Sciences, Kyusyu
University, Fukuoka, Japan.
Abstract
Psoriasis vulgaris is occasionally accompanied by autoimmune bullous
diseases, but the opposite is very rare. We document here the first
reported case of generalized pustular psoriasis that appeared during
steroid therapy for bullous pemphigoid. The serum cytokine levels and
the results of an immunohistochemical study over the disease course
suggest that the immunological state was consistent with a shift from
Th2-dominance to Th1-dominance. IL-17-producing cells appeared in the
skin lesions when each disease was most exacerbated and disappeared
after remission. Thus, the present case demonstrated a dynamic
immunological state in which the appearances of Th1 and Th2 as well as
Th17 varied during the course of the disease.
PMID: 19059833
Free full text
http://www.jle.com/medline.md?issn=1167-1122&vol=19&iss=1&page=69
<down for maintenace>
Short LIVED payoff.. <G>
Maybe tomorrow i SCORE.... GOAL>...
Today it's working:
http://www.jle.com/en/revues/medecine/ejd/e-docs/00/04/45/C9/article.phtml
[...] Results
In the present case, IFN-γ was not detectable (< 0.1 IU/mL) in any of
the serum samples over the studied course of the disease (table 1).
Serum TNF-α was elevated at the time of the pustular psoriasis attack,
and subsequently remained at a detectable level even after the
remission (table 1). Immunohistochemical analysis showed that both
IL-4- and IL-17-producing cells, as well as Foxp3-positive cells, were
detected in the upper dermis of the skin from a bullous pemphigoid
lesion (figure 2). On the other hand, the specimen from the psoriasis
lesion showed no evidence of IL-4-producing cells or Foxp3+ cells.
There were IL-17-producing cells not only in the dermis, but also in
the epidermis. The skin specimen obtained at remission contained no
IL-4- or IL-17-producing cells, or Foxp3-positive cells. The
immunological dynamics over the course are summarized in table 1.
Table 1
<snip> see link for table:
[...] Discussion
We document the first reported case of generalized pustular psoriasis
accompanying bullous pemphigoid. Although there was no published
information available about the role of Th17 in autoimmune bullous
diseases, accumulating evidence suggests that Th17 cytokines,
including IL-22, play an important role in the pathogenesis of
psoriasis [14-16]. We have recently confirmed that IL-17-producing
lymphocytes were detected in the skin lesions of both bullous
pemphigoid and pemphigus vulgaris (manuscript in preparation). The
immunological profile of the present case was ideal to support the
hypothesis that the immunological dynamics in autoimmune diseases
should not be viewed as a one-dimensional interaction between Th1 and
Th2, but as a multiple-level interaction among Th1, Th2, Treg and
Th17.
The Th1/Th2 theory simply and elegantly explains various immunological
states in mice and humans [8]. However, this theory is not suitable
for understanding the pathogenesis of autoimmune diseases because the
mechanism of exacerbation and amelioration cannot be simply explained
as a switch from Th1 to Th2. Now we have information about two new
players involved in the multidirectional immunological reactions:
i.e., Treg and Th17. Accumulated evidence suggests that Treg is
responsible for the third direction of an immunological reaction, and
controls autoimmunity, tumor immunity and resolution of immune
reactions. Th17 is accepted as a helper/effector cell subset
responsible for cytotoxic reactions in autoimmunity, a function that
could not be assigned by the Th1/Th2 hypothesis.
The role of Th17 in the lesional skin in bullous pemphigoid is
unknown, but they may have a similar effector function to the one they
have in several other autoimmune diseases. It is also conceivable that
lesional Th17 may not be a cause but a result of the disease: i.e.,
they may function in a non-specific protective and repair response
following damage in the epidermis. It would be valuable to elucidate
the precise mode of function of Th17.
It is, naturally, a limitation of this study that the immune
parameters investigated in a single patient do not provide sufficient
information to draw specific conclusions on the immune profile of
autoimmune diseases. Nevertheless, the multidimensional immune
reactions described here will help us to understand the pathogenesis
of autoimmune diseases and to discover new therapies.
<snip>
So... lacking IFN makes it's pustular in bEING? Or is part of ppp
pathways?
Maybe it's just one gene on the mhc II ... card14 and NO mutation?
Can we get Katherine Jordan to figure it out in Anne Bowcocks LAB?
<hint.. LOL> <w>
And back to kenya or kenda or whichever HONDA i'm looking at.
<is that 1675 + (see below) plus abstracts more then one K. honda? I
hope to SHOUT.. LOL>
And since it's Japanese we go with THE most respected and add in TRUE
Gut immunities + culprits.
http://www.ncbi.nlm.nih.gov/pubmed?term=honda%20SFB%20Th17
Good OLD Kenya [or Kenda? or both? or ER er er:]... Honda
ok.. since Kenyas' been with Littman and Ivanov, and it's immune and
gut and we already know the key players's.
WE stay with the scintifically prodigous Kenya Honda
Or is this the WONG Honda?
http://www.immunol.m.u-tokyo.ac.jp/page%20files/Takayanagi-Lab.html
http://www.sysbio.jst.go.jp/e/sakigake3/saki_11.html
http://www.med.osaka-u.ac.jp/eng/activities/results/2009/007.html
Duh... so is it KENDA? why why why? cause!
induction of Instestinal Th17 full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796826/
1676 (see above) - Honda K[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Honda%20K%5BAuthor%5D
#13 of 1676 (has Ivanov)
But this has a picture:
http://www.microbiology.columbia.edu/faculty/ivanov.html
<g>
And enlarged SFB shots in the ileum
http://www.microbiology.columbia.edu/faculty/images/figure1_ivanov.jpg
http://www.microbiology.columbia.edu/faculty/images/figure2_ivanov.jpg
13.- http://www.ncbi.nlm.nih.gov/pubmed/23084918
Intestinal commensal microbes as immune modulators.
Ivanov II, Honda K.
Cell Host Microbe. 2012 Oct 18;12(4):496-508. doi: 10.1016/j.chom.
2012.09.009.
PMID: 23084918
And with BAD BOY or good boy depending on the CAST : clostridium +
honda
4 hits -
http://www.ncbi.nlm.nih.gov/pubmed?term=Honda%20K%5BAuthor%5D%20clostridium
And this game is a FOOT, watson:
Or an ARM on what's your name again?
http://www.ncbi.nlm.nih.gov/pubmed/22673877
Curr Opin Immunol. 2012 Aug;24(4):392-7. doi: 10.1016/j.coi.
2012.05.007. Epub 2012 Jun 4.
The induction of Treg cells by gut-indigenous Clostridium.
Nagano Y, Itoh K, Honda K.
Source
Department of Immunology, Graduate School of Medicine, The University
of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Abstract
Foxp3+ CD4+ cells are prominent immune regulatory T (Treg) cells that
are most abundant in the intestine. Recent studies have suggested that
intestinal Treg cells consist of thymically and extrathymically
developed cells that have unique characteristics. A fraction of
intestinal Treg cells express T cell receptors that recognize antigens
that are derived from the gut microbiota. The presence of the gut
microbiota, particularly the Clostridium species, affects the
development and function of Treg cells. These intestinal bacteria-
induced Treg cells are likely to play a role in the tolerance toward
the gut microbiota. These recent advances provide new insight into how
T cells are educated in the intestine to maintain homeostasis with the
gut microbiota.
PMID: 22673877
And #2 of 4 has SFB + clostridia
so a Th1 skew (Th17) in the small intestine and a Th2 (foxp3- IL-10 et
al) in the colon.
Oddly enough you'd expect homeostasis in this situation perhaps? LoL
http://www.ncbi.nlm.nih.gov/pubmed/22527722
Cell Mol Life Sci. 2012 Nov;69(21):3635-50. doi: 10.1007/
s00018-012-0993-6. Epub 2012 Apr 22.
Immunoregulation by the gut microbiota.
Nishio J, Honda K.
Source
Department of Immunology, Graduate School of Medicine, The University
of Tokyo, Tokyo, 113-0033, Japan.
Abstract
The human intestinal mucosa is constantly exposed to commensal
microbiota. Since the gut microbiota is beneficial to the host, hosts
have evolved intestine-specific immune systems to co-exist with the
microbiota. On the other hand, the intestinal microbiota actively
regulates the host's immune system, and recent studies have revealed
that specific commensal bacterial species induce the accumulation of
specific immune cell populations. For instance, segmented filamentous
bacteria and Clostridium species belonging to clusters XIVa and IV
induce the accumulation of Th17 cells in the small intestine and
Foxp3(+) regulatory T cells in the large intestine, respectively. The
immune cells induced by the gut microbiota likely contribute to
intestinal homeostasis and influence systemic immunity in the host.
PMID: 22527722
#3 of 4 has been posted twice in this group:
PMID: 21205640
aND NOW Thrice:
http://www.ncbi.nlm.nih.gov/pubmed/21205640
#4 is staph related from 1994:
PMID: 8045913
OK.and what does it mean?
I know.. and i'm not telling.. LOL
But it was FUN...
Will see what LITTMAN is doing next:
And three hits: LIttman and SFB (2 with Ivanov and one with HONDA)
http://www.ncbi.nlm.nih.gov/pubmed?term=littman%20sfb
PMID: 21925113 (#1 of 3)
has
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209701/figure/F4/
And most recently as it looks like something might be up in a few days
or for xmas? LOL
Oh looky... he's got a cure... or pathway to one.
And that would be a huge LUMP of coal for big Pharma... LOL
http://www.ncbi.nlm.nih.gov/pubmed/23021777
Cell. 2012 Oct 12;151(2):289-303. doi: 10.1016/j.cell.2012.09.016.
Epub 2012 Sep 25.
A validated regulatory network for th17 cell specification.
Ciofani M, Madar A, Galan C, Sellars M, Mace K, Pauli F, Agarwal A,
Huang W, Parkurst CN, Muratet M, Newberry KM, Meadows S, Greenfield A,
Yang Y, Jain P, Kirigin FK, Birchmeier C, Wagner EF, Murphy KM, Myers
RM, Bonneau R, Littman DR.
Source
Molecular Pathogenesis Program, The Kimmel Center for Biology and
Medicine of the Skirball Institute, New York University School of
Medicine, New York, NY 10016, USA.
Abstract
Th17 cells have critical roles in mucosal defense and are major
contributors to inflammatory disease. Their differentiation requires
the nuclear hormone receptor RORγt working with multiple other
essential transcription factors (TFs). We have used an iterative
systems approach, combining genome-wide TF occupancy, expression
profiling of TF mutants, and expression time series to delineate the
Th17 global transcriptional regulatory network. We find that
cooperatively bound BATF and IRF4 contribute to initial chromatin
accessibility and, with STAT3, initiate a transcriptional program that
is then globally tuned by the lineage-specifying TF RORγt, which plays
a focal deterministic role at key loci. Integration of multiple data
sets allowed inference of an accurate predictive model that we
computationally and experimentally validated, identifying multiple new
Th17 regulators, including Fosl2, a key determinant of cellular
plasticity. This interconnected network can be used to investigate new
therapeutic approaches to manipulate Th17 functions in the setting of
inflammatory disease.
PMID: 23021777
FULLTEXT
http://www.sciencedirect.com/science/article/pii/S0092867409012483
And some credit is due:
22 hits: Ciofani M[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Ciofani%20M%5BAuthor%5D
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
http://www.ncbi.nlm.nih.gov/pubmed/23151182
Curr Pharm Des. 2012 Nov 7.
The interplay between the gut immune system and microbiota in health
and disease: Nutraceutical intervention for restoring intestinal
homeostasis.
Magrone T, Jirillo E.
Source
Department of Medic Basic Sciences, Neuroscience and Sensory Organs,
University of Bari, Bari, Italy. thea.m...@libero.it.
Abstract
Gut immune system is daily exposed to a plethora of antigens contained
in the environment as well as in food. Both secondary lymphoid tissue,
such as Peyers patches, and lymphoid follicles (tertiary lymphoid
tissue) are able to respond to antigenic stimuli releasing cytokines
or producing antibodies (secretory IgA). Intestinal epithelial cells
are in close cooperation with intraepithelial lymphocytes and possess
Toll-like receptors on their surface and Nod-like receptors (NLRs)
which sense pathogens or pathogen-associated molecular patterns.
Intestinal microbiota, mainly composed by Bacteroidetes and
Firmicutes, generates tolerogenic response acting on gut dendritic
cells and inhibiting the T helper (h)-17 cells anti-inflammatory
pathway. This is the case of Bacteroides fragilis which leads to the
production of interleukin-10, an anti-inflammatory cytokine from both
T regulatory cells and lamina propria macrophages. Conversely,
segmented filamentous bacteria rather induce Th17 cells, thus
promoting intestinal inflammation. Intestinal microbiota and its toxic
components have been shown to act on both Nod1 and Nod2 receptors and
their defective signaling account for the development of inflammatory
bowel disease (IBD). In IBD a loss of normal tolerance to intestinal
microbiota seems to be the main trigger of mucosal damage. In
addition, intestinal microbiota thanks to its regulatory function of
gut immune response can prevent or retard neoplastic growth. In fact,
chronic exposure to environmental microorganisms seems to be
associated with low frequency of cancer risk. Major nutraceuticals or
functional foods employed in the modulation of intestinal microbiota
are represented by prebiotics, probiotics, polyunsaturated fatty
acids, amino acids and polyphenols. The cellular and molecular effects
performed by these natural products in terms of modulation of the
intestinal microbiota and mostly attenuation of the inflammatory
pathway are described.
PMID: 23151182
++++++++++++++++++++++++++++++++
Curr Opin Immunol. 2012 Aug;24(4):385-91. doi: 10.1016/j.coi.
2012.04.009. Epub 2012 May 19.
T cell tolerance and immunity to commensal bacteria.
Nutsch KM, Hsieh CS.
Source
Department of Medicine, Division of Rheumatology, Washington
University School of Medicine, St. Louis, MO 63110, United States.
Abstract
The commensal bacteria normally resident in the gastrointestinal tract
represent an enormous pool of foreign antigen within the body.
Although mechanical barriers limit entry of bacteria into the host,
recent data suggest that T cells routinely interact with commensal
bacteria using both antigen-specific and non-specific receptors.
Depending on the bacterial species, either regulatory or effector T
cell responses can be generated. For example, segmented filamentous
bacteria (SFB) favor effector Th17 responses whereas Bacteroides
fragilis and certain Clostridium species favor Foxp3+ regulatory T
(Treg) cell responses. Thus, in contrast with the notion that only
tolerogenic responses are required to self, gut homeostasis may
require both tolerance and immunity to various constituents of the
commensal microbiota.
PMID: 22613090 [PubMed - in process]
PMCID: PMC3423487
[Available on 2013/8/1]
-----------
www.hindawi.com/journals/ijhep/aip/439024.pdf
Sung, Lee and El-Nezami: Bacteria in the treatment of liver cancer1
Title: Regulation of T helper 17 (TH17) by bacteria: An approach for
the treatment of 1 hepatocellular carcinoma 2
Full author names: Cecilia Ying Ju Sung 1, Nikki Pui-yue Lee2, Hani El-
Nezami1
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
OK and like last night.. i'm bored now.. LOL
Will i cure pancan and cancer soon?
I hope..
All we have to do is slow that clostridia from making excess TREGs and
funking up p53 (tp53 -tumor protein 53).
Now that is somewhat more important then a rash.. LOL
But to not be RASH i'm also working hard on autoimmunities and SFB and
L. Plantarum and a few dozen
gene's and microbiota we oughta to control Gut homeostasis.
So there..
Live and let live unless it's commensal flora that isn't playing fair.
and Being a BULLY to other commensal flora.
and ... you don't like not being NORMAL> duh
randall... and i hope to NOT bully BB...as he's a kewl person and
making this group work BETTER...
NOT for BB if he can choose to NOT OPEN this.
Not sure how BB Does that but i've stopped posting so we can work it
OUT. :)
And thus i start a new thread:
The old thread:
link:
Thurs, Dec 6 2012 6:42 pm
Subject: Re: A dietary psoriasis treatment
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/204a20b22275d0e1
you said in the ABOVE thread:
------------
FromTheRafters
View profile
More options Dec 6, 6:42 pm
JRStern used his keyboard to write :
- Hide quoted text -
> On Wed, 05 Dec 2012 20:11:54 -0500, FromTheRafters
> <erra...@nomail.afraid.org> wrote:
>> JRStern wrote :
>>> On Mon, 3 Dec 2012 23:23:02 -0800 (PST), randall <ranhu...@aol.com>
>>> wrote:
>>>> OK, so what tips the SCALEs for you, more then say curcumin?
>>> My curcumin cocktail with fish oil and vitamin C, and now with black
>>> pepper, plus mass quantities of Curel, and also now using Dove
>>> moisturizing body wash instead of previous more harsh soaps. I'm not
>>> clear, nothing has cleared me since I got this thing, but this
>>> regimen, and long-sleeve shirts, keep me up and moving about in the
>>> world.
>> How long has this flare-up lasted, if you don't mind my asking? Also,
>> if you've had more than one flare-up - how long was the remission
>> period?
>> [...]
> Never had a clearing in 20+ years.
> Not what I wanted to hear, I'm newly diagnosed and still have hopes of
> lengthy remission.
> Within the chronic condition I've had flare-ups that slowly trained me
> as to ways to avoid them and guided me towards better maintenance
> strategies.
Hopefully I can get to recognize my triggers and learn to avoid them
too. For now it's visits to the easy-bake oven and smearing
clobetasol
on the affected areas. I really don't want pills or shots, but it may
come to that.
Thanks for replying, I wasn't sure if my choice of NNTP server was
blocked in this group.
---------------------------
Thus:
Does this help BB to figure out HOW not to OPEN my THREADS?
I will start my OWN group and then use links to THESE LONG posts chock
a block
full of pubmed ABSTRACTS....
Which... IMO... science DOES matter... (<G><w>)
http://en.wikipedia.org/wiki/NNTP
http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
And will bohgosity cop to which of these he's using?
http://en.wikipedia.org/wiki/Comparison_of_Usenet_newsreaders
So we know how this works?
Maybe FromtheRAFTERs can tell us or me?
and RAFTER and his PPP
If/When you onset with pustular there had to BE a Trigger.
Or so we've been led to believe.
So once it happens an epicgenetic event onsets that doesn't change in
the course of having psoriasis almost 100% of the time..
Unless you use TNF blocker's till the day you expire..
The trigger:
Something like antibiotics or STREP (candida et al) for instance.
Noticed - rafter --> ppp- link:
http://www.everydayhealth.com/psoriasis/living-with-pustular-psoriasis.aspx
If it had been hpa-axis susan the game would be a FOOT. LoL
Elementary as i'm watching it.. LOL
<I was doing this last night while enjoying sherlock "elementary" and
cute watson [ lucy Liu])
http://www.huffingtonpost.com/2012/09/27/elementary-lucy-liu_n_1919614.html
ok enough of that segue..but but but...
yes id squid?
Well doesn't her left eye look oriental and her RIGHT eye look
westernized if there
be such a non symmetrical thingy pooh?
I don't know id squid.. good question.. will think it over and OUT..
LOL
----------------
ok..carry on tar baby..
Does affected skin look like this:
http://upload.wikimedia.org/wikipedia/en/9/91/Acute_generalized_exanthematous_pustulosis.jpg
http://en.wikipedia.org/wiki/Acute_generalized_exanthematous_pustulosis
Acute generalized exanthematous pustulosis (AGEP) (also known as
"Pustular drug eruption," and "Toxic pustuloderma") is a not uncommon
cutaneous reaction pattern that in 90% of cases is related to
medication administration, characterized by a sudden eruption that
appears on average five days after the medication is started.[1]:124
It is mediated by T cells.[2]
Presentation
AGEP is an acute febrile drug eruption characterized by numerous
small, primarily non-follicular, sterile pustules, arising within
large areas of edematous erythema.[3]
The eruption follows a self-limiting course and will end before a week
provided the causative agent (e.g. medication) is discarded. It is
accompanied by fever, neutrophilia, and sometimes by facial edema,
hepatitis and eosinophilia. The mortality rate is about 5% and the
differential diagnosis includes Stevens–Johnson syndrome (SJS).
Contrary to SJS, in AGEP, mucosa are not affected, which means that
there are no blisters in the mouth or vagina.
Treatment
The treatment is (1) stop the offending drug (antibiotics), (2)
symptomatic (fever) and (3) for complications (hepatitis).[4]
<snip>
ppp
http://en.wikipedia.org/wiki/Pustulosis
Pustulosis is highly inflammatory skin condition resulting in large
fluid-filled blister-like areas - pustules. Pustulosis typically
occurs on the palms of the hands and/or the soles of the feet. The
skin of these areas peels and flakes (exfoliates).[1] This condition-
also referred to as "palmo-plantar pustulosis" - is a feature of
pustular psoriasis.
Pustular - 1,080 hits- p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=+pustular&start=0&
ppp - 145 hits - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=ppp&start=0&
palmoplantar pustular psoriasis - 17 hit -p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=palmoplantar+pustular+psoriasis&start=0&
1340 all groups
https://groups.google.com/groups/search?qt_s=1&q=palmoplantar+pustular+psoriasis
http://en.wikipedia.org/wiki/Pustulosis_palmaris_et_plantaris
Pustulosis palmaris et plantaris (also known as "Pustulosis of palms
and soles,"[1] "Palmoplantar pustulosis," "Persistent palmoplantar
pustulosis," "Pustular psoriasis of the Barber type," and "Pustular
psoriasis of the extremities") is a chronic recurrent pustular
dermatosis localized on the palms and soles only, characterized
histologically by intraepidermal vesicles filled with neutrophils.[2]:
411,628[3]:204
<snip>
1091 hits - psoria* + pustular - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20pustular
http://www.ncbi.nlm.nih.gov/pubmed/22426986
Serum and tissue levels of IL-17 in different clinical subtypes of
psoriasis.
Yilmaz SB, Cicek N, Coskun M, Yegin O, Alpsoy E.
Source
Department of Dermatology and Venereology, Akdeniz University School
of Medicine, Antalya, Turkey.
Abstract
Serum IL-17 levels and IL-17 mRNA expression have been reported to be
higher in psoriatic skin than normal skin. There are very limited data
in the literature about difference in the levels of this cytokine in
various clinical disease subtypes. We aimed to evaluate whether there
is a difference in the level of this cytokine according to clinical
subtypes of psoriasis. 70 psoriasis patients (30 plaque psoriasis, 20
guttate psoriasis, and 20 pustular psoriasis) and 50 age- and sex-
matched healthy volunteers were included in the study. Serum IL-17
levels were determined by ELISA. Skin biopsies obtained from lesions
and non-lesional skin area of 12 patients and healthy individuals (n =
5) were analyzed by quantitative PCR (qPCR) to measure the mRNA levels
of IL-17. Statistically, the serum IL-17 levels did not exhibit any
difference between the patients and control groups. However, analysis
of each subgroup revealed that the IL-17 levels were significantly
higher in pustular psoriasis group (10.09 ± 12.6 pg/ml) than controls
(4.4 ± 4.1 pg/ml) (p = 0.02). In addition, the IL-17 levels of plaque
psoriasis patients with PASI score ≥10 (11.30 ± 6.0 pg/ml) were
significantly higher than that of patients with PASI score <10 (3.39 ±
2.6 pg/ml) and controls (p < 0.001). The Pearson correlation analysis
showed a positive correlation between the serum IL-17 levels and PASI.
Lesional skin samples of psoriasis patients showed significantly
higher levels of IL-17 mRNA compared with perilesional skin samples (p
= 0.017). Also, in the pustular psoriasis, IL-17 mRNA levels were
found to be distinctively high in comparison with other clinical
subtypes and healthy controls. Our results indicate that IL-17 and
Th17 cells have an important role in pustular psoriasis and severe
psoriasis.
PMID: 22426986
And a heart FELT cardio delight:
http://www.ncbi.nlm.nih.gov/pubmed/19661531
J Rheumatol Suppl. 2009 Aug;83:19-20.
Clinical aspects and comorbidities of psoriasis.
Ayala F, Ayala F.
Source
Division of Dermatology, Department of Systematic Pathology,
University of Naples Federico II, I 80131 Naples, Italy.
Abstract
Psoriasis is a disease mediated by Th1 and Th17 cytokines that has
different phenotypes (plaque, guttate, pustular, and erythrodermic
type). Aside from the well known psoriatic arthritis, associated
disorders may occur more frequently than expected, including Crohn's
disease, anxiety/depression, and metabolic syndrome. This is based on
a constellation of different factors, including abdominal obesity,
atherogenic dyslipidemia, hypertension, and glucose intolerance, and
is a strong predictor of type 2 diabetes, cardiovascular disease, and
stroke. People with moderate to severe psoriasis have more risk for
cardiac disease, presumably due to the inflammatory nature of
psoriasis, causing inflammatory changes in coronary arteries. The
strong association between psoriasis and obesity potentially makes
psoriasis an important healthcare issue. Since cardiovascular risk
factors are higher in psoriatic patients, dermatologists treating
moderate to severe psoriasis should screen for their presence, thus
approaching psoriasis as a potential multisystem disorder.
PMID: 19661531
And since this next one has a full text i'm having a little FUN.
now
http://www.ncbi.nlm.nih.gov/pubmed/19059833
Eur J Dermatol. 2009 Jan-Feb;19(1):69-71. Epub 2008 Dec 5.
Bullous pemphigoid followed by pustular psoriasis showing Th1, Th2,
Treg and Th17 immunological changes.
Yasukawa S, Dainichi T, Kokuba H, Moroi Y, Urabe K, Hashimoto T, Furue
M.
Source
Department of Dermatology, Graduate School of Medical Sciences, Kyusyu
University, Fukuoka, Japan.
Abstract
Psoriasis vulgaris is occasionally accompanied by autoimmune bullous
diseases, but the opposite is very rare. We document here the first
reported case of generalized pustular psoriasis that appeared during
steroid therapy for bullous pemphigoid. The serum cytokine levels and
the results of an immunohistochemical study over the disease course
suggest that the immunological state was consistent with a shift from
Th2-dominance to Th1-dominance. IL-17-producing cells appeared in the
skin lesions when each disease was most exacerbated and disappeared
after remission. Thus, the present case demonstrated a dynamic
immunological state in which the appearances of Th1 and Th2 as well as
Th17 varied during the course of the disease.
PMID: 19059833
Free full text
http://www.jle.com/medline.md?issn=1167-1122&vol=19&iss=1&page=69
<down for maintenace>
Short LIVED payoff.. <G>
Maybe tomorrow i SCORE.... GOAL>...
Today it's working:
http://www.jle.com/en/revues/medecine/ejd/e-docs/00/04/45/C9/article.phtml
[...] Results
In the present case, IFN-γ was not detectable (< 0.1 IU/mL) in any of
the serum samples over the studied course of the disease (table 1).
Serum TNF-α was elevated at the time of the pustular psoriasis attack,
and subsequently remained at a detectable level even after the
remission (table 1). Immunohistochemical analysis showed that both
IL-4- and IL-17-producing cells, as well as Foxp3-positive cells, were
detected in the upper dermis of the skin from a bullous pemphigoid
lesion (figure 2). On the other hand, the specimen from the psoriasis
lesion showed no evidence of IL-4-producing cells or Foxp3+ cells.
There were IL-17-producing cells not only in the dermis, but also in
the epidermis. The skin specimen obtained at remission contained no
IL-4- or IL-17-producing cells, or Foxp3-positive cells. The
immunological dynamics over the course are summarized in table 1.
Table 1
<snip> see link for table:
[...] Discussion
We document the first reported case of generalized pustular psoriasis
accompanying bullous pemphigoid. Although there was no published
information available about the role of Th17 in autoimmune bullous
diseases, accumulating evidence suggests that Th17 cytokines,
including IL-22, play an important role in the pathogenesis of
psoriasis [14-16]. We have recently confirmed that IL-17-producing
lymphocytes were detected in the skin lesions of both bullous
pemphigoid and pemphigus vulgaris (manuscript in preparation). The
immunological profile of the present case was ideal to support the
hypothesis that the immunological dynamics in autoimmune diseases
should not be viewed as a one-dimensional interaction between Th1 and
Th2, but as a multiple-level interaction among Th1, Th2, Treg and
Th17.
The Th1/Th2 theory simply and elegantly explains various immunological
states in mice and humans [8]. However, this theory is not suitable
for understanding the pathogenesis of autoimmune diseases because the
mechanism of exacerbation and amelioration cannot be simply explained
as a switch from Th1 to Th2. Now we have information about two new
players involved in the multidirectional immunological reactions:
i.e., Treg and Th17. Accumulated evidence suggests that Treg is
responsible for the third direction of an immunological reaction, and
controls autoimmunity, tumor immunity and resolution of immune
reactions. Th17 is accepted as a helper/effector cell subset
responsible for cytotoxic reactions in autoimmunity, a function that
could not be assigned by the Th1/Th2 hypothesis.
The role of Th17 in the lesional skin in bullous pemphigoid is
unknown, but they may have a similar effector function to the one they
have in several other autoimmune diseases. It is also conceivable that
lesional Th17 may not be a cause but a result of the disease: i.e.,
they may function in a non-specific protective and repair response
following damage in the epidermis. It would be valuable to elucidate
the precise mode of function of Th17.
It is, naturally, a limitation of this study that the immune
parameters investigated in a single patient do not provide sufficient
information to draw specific conclusions on the immune profile of
autoimmune diseases. Nevertheless, the multidimensional immune
reactions described here will help us to understand the pathogenesis
of autoimmune diseases and to discover new therapies.
<snip>
So... lacking IFN makes it's pustular in bEING? Or is part of ppp
pathways?
Maybe it's just one gene on the mhc II ... card14 and NO mutation?
Can we get Katherine Jordan to figure it out in Anne Bowcocks LAB?
<hint.. LOL> <w>
And back to kenya or kenda or whichever HONDA i'm looking at.
<is that 1675 + (see below) plus abstracts more then one K. honda? I
hope to SHOUT.. LOL>
And since it's Japanese we go with THE most respected and add in TRUE
Gut immunities + culprits.
http://www.ncbi.nlm.nih.gov/pubmed?term=honda%20SFB%20Th17
Good OLD Kenya [or Kenda? or both? or ER er er:]... Honda
ok.. since Kenyas' been with Littman and Ivanov, and it's immune and
gut and we already know the key players's.
WE stay with the scintifically prodigous Kenya Honda
Or is this the WONG Honda?
http://www.immunol.m.u-tokyo.ac.jp/page%20files/Takayanagi-Lab.html
http://www.sysbio.jst.go.jp/e/sakigake3/saki_11.html
http://www.med.osaka-u.ac.jp/eng/activities/results/2009/007.html
Duh... so is it KENDA? why why why? cause!
induction of Instestinal Th17 full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796826/
1676 (see above) - Honda K[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Honda%20K%5BAuthor%5D
#13 of 1676 (has Ivanov)
But this has a picture:
http://www.microbiology.columbia.edu/faculty/ivanov.html
<g>
And enlarged SFB shots in the ileum
http://www.microbiology.columbia.edu/faculty/images/figure1_ivanov.jpg
http://www.microbiology.columbia.edu/faculty/images/figure2_ivanov.jpg
13.- http://www.ncbi.nlm.nih.gov/pubmed/23084918
Intestinal commensal microbes as immune modulators.
Ivanov II, Honda K.
Cell Host Microbe. 2012 Oct 18;12(4):496-508. doi: 10.1016/j.chom.
2012.09.009.
PMID: 23084918
And with BAD BOY or good boy depending on the CAST : clostridium +
honda
4 hits -
http://www.ncbi.nlm.nih.gov/pubmed?term=Honda%20K%5BAuthor%5D%20clostridium
And this game is a FOOT, watson:
Or an ARM on what's your name again?
http://www.ncbi.nlm.nih.gov/pubmed/22673877
Curr Opin Immunol. 2012 Aug;24(4):392-7. doi: 10.1016/j.coi.
2012.05.007. Epub 2012 Jun 4.
The induction of Treg cells by gut-indigenous Clostridium.
Nagano Y, Itoh K, Honda K.
Source
Department of Immunology, Graduate School of Medicine, The University
of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Abstract
Foxp3+ CD4+ cells are prominent immune regulatory T (Treg) cells that
are most abundant in the intestine. Recent studies have suggested that
intestinal Treg cells consist of thymically and extrathymically
developed cells that have unique characteristics. A fraction of
intestinal Treg cells express T cell receptors that recognize antigens
that are derived from the gut microbiota. The presence of the gut
microbiota, particularly the Clostridium species, affects the
development and function of Treg cells. These intestinal bacteria-
induced Treg cells are likely to play a role in the tolerance toward
the gut microbiota. These recent advances provide new insight into how
T cells are educated in the intestine to maintain homeostasis with the
gut microbiota.
PMID: 22673877
And #2 of 4 has SFB + clostridia
so a Th1 skew (Th17) in the small intestine and a Th2 (foxp3- IL-10 et
al) in the colon.
Oddly enough you'd expect homeostasis in this situation perhaps? LoL
http://www.ncbi.nlm.nih.gov/pubmed/22527722
Cell Mol Life Sci. 2012 Nov;69(21):3635-50. doi: 10.1007/
s00018-012-0993-6. Epub 2012 Apr 22.
Immunoregulation by the gut microbiota.
Nishio J, Honda K.
Source
Department of Immunology, Graduate School of Medicine, The University
of Tokyo, Tokyo, 113-0033, Japan.
Abstract
The human intestinal mucosa is constantly exposed to commensal
microbiota. Since the gut microbiota is beneficial to the host, hosts
have evolved intestine-specific immune systems to co-exist with the
microbiota. On the other hand, the intestinal microbiota actively
regulates the host's immune system, and recent studies have revealed
that specific commensal bacterial species induce the accumulation of
specific immune cell populations. For instance, segmented filamentous
bacteria and Clostridium species belonging to clusters XIVa and IV
induce the accumulation of Th17 cells in the small intestine and
Foxp3(+) regulatory T cells in the large intestine, respectively. The
immune cells induced by the gut microbiota likely contribute to
intestinal homeostasis and influence systemic immunity in the host.
PMID: 22527722
#3 of 4 has been posted twice in this group:
PMID: 21205640
aND NOW Thrice:
http://www.ncbi.nlm.nih.gov/pubmed/21205640
#4 is staph related from 1994:
PMID: 8045913
OK.and what does it mean?
I know.. and i'm not telling.. LOL
But it was FUN...
Will see what LITTMAN is doing next:
And three hits: LIttman and SFB (2 with Ivanov and one with HONDA)
http://www.ncbi.nlm.nih.gov/pubmed?term=littman%20sfb
PMID: 21925113 (#1 of 3)
has
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209701/figure/F4/
And most recently as it looks like something might be up in a few days
or for xmas? LOL
Oh looky... he's got a cure... or pathway to one.
And that would be a huge LUMP of coal for big Pharma... LOL
http://www.ncbi.nlm.nih.gov/pubmed/23021777
Cell. 2012 Oct 12;151(2):289-303. doi: 10.1016/j.cell.2012.09.016.
Epub 2012 Sep 25.
A validated regulatory network for th17 cell specification.
Ciofani M, Madar A, Galan C, Sellars M, Mace K, Pauli F, Agarwal A,
Huang W, Parkurst CN, Muratet M, Newberry KM, Meadows S, Greenfield A,
Yang Y, Jain P, Kirigin FK, Birchmeier C, Wagner EF, Murphy KM, Myers
RM, Bonneau R, Littman DR.
Source
Molecular Pathogenesis Program, The Kimmel Center for Biology and
Medicine of the Skirball Institute, New York University School of
Medicine, New York, NY 10016, USA.
Abstract
Th17 cells have critical roles in mucosal defense and are major
contributors to inflammatory disease. Their differentiation requires
the nuclear hormone receptor RORγt working with multiple other
essential transcription factors (TFs). We have used an iterative
systems approach, combining genome-wide TF occupancy, expression
profiling of TF mutants, and expression time series to delineate the
Th17 global transcriptional regulatory network. We find that
cooperatively bound BATF and IRF4 contribute to initial chromatin
accessibility and, with STAT3, initiate a transcriptional program that
is then globally tuned by the lineage-specifying TF RORγt, which plays
a focal deterministic role at key loci. Integration of multiple data
sets allowed inference of an accurate predictive model that we
computationally and experimentally validated, identifying multiple new
Th17 regulators, including Fosl2, a key determinant of cellular
plasticity. This interconnected network can be used to investigate new
therapeutic approaches to manipulate Th17 functions in the setting of
inflammatory disease.
PMID: 23021777
FULLTEXT
http://www.sciencedirect.com/science/article/pii/S0092867409012483
And some credit is due:
22 hits: Ciofani M[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Ciofani%20M%5BAuthor%5D
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
http://www.ncbi.nlm.nih.gov/pubmed/23151182
Curr Pharm Des. 2012 Nov 7.
The interplay between the gut immune system and microbiota in health
and disease: Nutraceutical intervention for restoring intestinal
homeostasis.
Magrone T, Jirillo E.
Source
Department of Medic Basic Sciences, Neuroscience and Sensory Organs,
University of Bari, Bari, Italy. thea.m...@libero.it.
Abstract
Gut immune system is daily exposed to a plethora of antigens contained
in the environment as well as in food. Both secondary lymphoid tissue,
such as Peyers patches, and lymphoid follicles (tertiary lymphoid
tissue) are able to respond to antigenic stimuli releasing cytokines
or producing antibodies (secretory IgA). Intestinal epithelial cells
are in close cooperation with intraepithelial lymphocytes and possess
Toll-like receptors on their surface and Nod-like receptors (NLRs)
which sense pathogens or pathogen-associated molecular patterns.
Intestinal microbiota, mainly composed by Bacteroidetes and
Firmicutes, generates tolerogenic response acting on gut dendritic
cells and inhibiting the T helper (h)-17 cells anti-inflammatory
pathway. This is the case of Bacteroides fragilis which leads to the
production of interleukin-10, an anti-inflammatory cytokine from both
T regulatory cells and lamina propria macrophages. Conversely,
segmented filamentous bacteria rather induce Th17 cells, thus
promoting intestinal inflammation. Intestinal microbiota and its toxic
components have been shown to act on both Nod1 and Nod2 receptors and
their defective signaling account for the development of inflammatory
bowel disease (IBD). In IBD a loss of normal tolerance to intestinal
microbiota seems to be the main trigger of mucosal damage. In
addition, intestinal microbiota thanks to its regulatory function of
gut immune response can prevent or retard neoplastic growth. In fact,
chronic exposure to environmental microorganisms seems to be
associated with low frequency of cancer risk. Major nutraceuticals or
functional foods employed in the modulation of intestinal microbiota
are represented by prebiotics, probiotics, polyunsaturated fatty
acids, amino acids and polyphenols. The cellular and molecular effects
performed by these natural products in terms of modulation of the
intestinal microbiota and mostly attenuation of the inflammatory
pathway are described.
PMID: 23151182
++++++++++++++++++++++++++++++++
Curr Opin Immunol. 2012 Aug;24(4):385-91. doi: 10.1016/j.coi.
2012.04.009. Epub 2012 May 19.
T cell tolerance and immunity to commensal bacteria.
Nutsch KM, Hsieh CS.
Source
Department of Medicine, Division of Rheumatology, Washington
University School of Medicine, St. Louis, MO 63110, United States.
Abstract
The commensal bacteria normally resident in the gastrointestinal tract
represent an enormous pool of foreign antigen within the body.
Although mechanical barriers limit entry of bacteria into the host,
recent data suggest that T cells routinely interact with commensal
bacteria using both antigen-specific and non-specific receptors.
Depending on the bacterial species, either regulatory or effector T
cell responses can be generated. For example, segmented filamentous
bacteria (SFB) favor effector Th17 responses whereas Bacteroides
fragilis and certain Clostridium species favor Foxp3+ regulatory T
(Treg) cell responses. Thus, in contrast with the notion that only
tolerogenic responses are required to self, gut homeostasis may
require both tolerance and immunity to various constituents of the
commensal microbiota.
PMID: 22613090 [PubMed - in process]
PMCID: PMC3423487
[Available on 2013/8/1]
-----------
www.hindawi.com/journals/ijhep/aip/439024.pdf
Sung, Lee and El-Nezami: Bacteria in the treatment of liver cancer1
Title: Regulation of T helper 17 (TH17) by bacteria: An approach for
the treatment of 1 hepatocellular carcinoma 2
Full author names: Cecilia Ying Ju Sung 1, Nikki Pui-yue Lee2, Hani El-
Nezami1
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
OK and like last night.. i'm bored now.. LOL
Will i cure pancan and cancer soon?
I hope..
All we have to do is slow that clostridia from making excess TREGs and
funking up p53 (tp53 -tumor protein 53).
Now that is somewhat more important then a rash.. LOL
But to not be RASH i'm also working hard on autoimmunities and SFB and
L. Plantarum and a few dozen
gene's and microbiota we oughta to control Gut homeostasis.
So there..
Live and let live unless it's commensal flora that isn't playing fair.
and Being a BULLY to other commensal flora.
and ... you don't like not being NORMAL> duh
randall... and i hope to NOT bully BB...as he's a kewl person and
making this group work BETTER...
FromTheRafters
Dec 7, 2012, 8:53:26 PM12/7/12
to
randall expressed precisely :
Yep, I wrote that - not him.
attribution/indents.
weeks and realize some personality conflicts exist - it *is* usenet
after all.
usenet?
I had been doing for some years when all of a sudden in early June I
seemed to be wearing barbed-wire socks to work.
> If it had been hpa-axis susan the game would be a FOOT. LoL
>
> Elementary as i'm watching it.. LOL
>
> <I was doing this last night while enjoying sherlock "elementary" and
> cute watson [ lucy Liu])
>
> http://www.huffingtonpost.com/2012/09/27/elementary-lucy-liu_n_1919614.html
...and *now* back to our regularly scheduled program.
[...]
> ----------------
>
> ok..carry on tar baby..>
>
> Does affected skin look like this:
> http://upload.wikimedia.org/wikipedia/en/9/91/Acute_generalized_exanthematous_pustulosis.jpg
>
Those little raised white spots can be found on my hands, but my feet
had larger blisters than that and they looked a lot like hamburger
patties with toes.
Thanks for the links, I'll get to the rest of them later as I can't sit
for long. It seems like the blood pressure hurts my feet when I'm
sitting or standing.
[...]
>
>> Within the chronic condition I've had flare-ups that slowly trained me
>> as to ways to avoid them and guided me towards better maintenance
>> strategies.
>
Nope, I didn't write that - he did. Somehow you must have messed up the
>> Within the chronic condition I've had flare-ups that slowly trained me
>> as to ways to avoid them and guided me towards better maintenance
>> strategies.
>
attribution/indents.
>
> Hopefully I can get to recognize my triggers and learn to avoid them
> too. For now it's visits to the easy-bake oven and smearing
> clobetasol
> on the affected areas. I really don't want pills or shots, but it may
> come to that.
> Thanks for replying, I wasn't sure if my choice of NNTP server was
> blocked in this group.
>
> ---------------------------
>
>
> Thus:
>
> Does this help BB to figure out HOW not to OPEN my THREADS?
I can't say that I care about that. I've read the group for a couple of
> Hopefully I can get to recognize my triggers and learn to avoid them
> too. For now it's visits to the easy-bake oven and smearing
> clobetasol
> on the affected areas. I really don't want pills or shots, but it may
> come to that.
> Thanks for replying, I wasn't sure if my choice of NNTP server was
> blocked in this group.
>
> ---------------------------
>
>
> Thus:
>
> Does this help BB to figure out HOW not to OPEN my THREADS?
weeks and realize some personality conflicts exist - it *is* usenet
after all.
>
> I will start my OWN group and then use links to THESE LONG posts chock
> a block
> full of pubmed ABSTRACTS....
>
> Which... IMO... science DOES matter... (<G><w>)
>
>
> http://en.wikipedia.org/wiki/NNTP
> http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
>
> And will bohgosity cop to which of these he's using?
> http://en.wikipedia.org/wiki/Comparison_of_Usenet_newsreaders
Why/how would that matter? How does "view profile" relate to me in
> I will start my OWN group and then use links to THESE LONG posts chock
> a block
> full of pubmed ABSTRACTS....
>
> Which... IMO... science DOES matter... (<G><w>)
>
>
> http://en.wikipedia.org/wiki/NNTP
> http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
>
> And will bohgosity cop to which of these he's using?
> http://en.wikipedia.org/wiki/Comparison_of_Usenet_newsreaders
usenet?
>
> So we know how this works?
How *what* works?
> So we know how this works?
>
> Maybe FromtheRAFTERs can tell us or me?
I'd probably try if I knew what you were going on about.
> Maybe FromtheRAFTERs can tell us or me?
>
> and RAFTER and his PPP
>
> If/When you onset with pustular there had to BE a Trigger.
>
> Or so we've been led to believe.
Do you doubt this? For myself, I was doing nothing different from what
> and RAFTER and his PPP
>
> If/When you onset with pustular there had to BE a Trigger.
>
> Or so we've been led to believe.
I had been doing for some years when all of a sudden in early June I
seemed to be wearing barbed-wire socks to work.
>
> So once it happens an epicgenetic event onsets that doesn't change in
> the course of having psoriasis almost 100% of the time..
> Unless you use TNF blocker's till the day you expire..
>
> The trigger:
>
> Something like antibiotics or STREP (candida et al) for instance.
>
> Noticed - rafter --> ppp- link:
> http://www.everydayhealth.com/psoriasis/living-with-pustular-psoriasis.aspx
>
Not a very uplifting story as I recall.
> So once it happens an epicgenetic event onsets that doesn't change in
> the course of having psoriasis almost 100% of the time..
> Unless you use TNF blocker's till the day you expire..
>
> The trigger:
>
> Something like antibiotics or STREP (candida et al) for instance.
>
> Noticed - rafter --> ppp- link:
> http://www.everydayhealth.com/psoriasis/living-with-pustular-psoriasis.aspx
>
> If it had been hpa-axis susan the game would be a FOOT. LoL
>
> Elementary as i'm watching it.. LOL
>
> <I was doing this last night while enjoying sherlock "elementary" and
> cute watson [ lucy Liu])
>
> http://www.huffingtonpost.com/2012/09/27/elementary-lucy-liu_n_1919614.html
[...]
> ----------------
>
> ok..carry on tar baby..>
>
> Does affected skin look like this:
> http://upload.wikimedia.org/wikipedia/en/9/91/Acute_generalized_exanthematous_pustulosis.jpg
>
had larger blisters than that and they looked a lot like hamburger
patties with toes.
Thanks for the links, I'll get to the rest of them later as I can't sit
for long. It seems like the blood pressure hurts my feet when I'm
sitting or standing.
[...]
randall
Dec 8, 2012, 7:16:52 PM12/8/12
to
On Dec 7, 5:53 pm, FromTheRafters <erra...@nomail.afraid.org> wrote:
> randall expressed precisely :
>
>
> > hey
>
> > NOT for BB if he can choose to NOT OPEN this.
>
> > Not sure how BB Does that but i've stopped posting so we can work it
> > OUT. :)
>
> > And thus i start a new thread:
>
> > The old thread:
>
> > link:
> > Thurs, Dec 6 2012 6:42 pm
> > Subject: Re: A dietary psoriasis treatment
> >http://groups.google.com/group/alt.support.skin-diseases.psoriasis/ms...
> randall expressed precisely :
>
>
> > hey
>
> > NOT for BB if he can choose to NOT OPEN this.
>
> > Not sure how BB Does that but i've stopped posting so we can work it
> > OUT. :)
>
> > And thus i start a new thread:
>
> > The old thread:
>
> > link:
> > Thurs, Dec 6 2012 6:42 pm
> > Subject: Re: A dietary psoriasis treatment
>
> > Hopefully I can get to recognize my triggers and learn to avoid them
> > too. For now it's visits to the easy-bake oven and smearing
> > clobetasol
> > on the affected areas. I really don't want pills or shots, but it may
> > come to that.
> > Thanks for replying, I wasn't sure if my choice of NNTP server was
> > blocked in this group.
>
> > ---------------------------
>
> > Thus:
>
> > Does this help BB to figure out HOW not to OPEN my THREADS?
>
> I can't say that I care about that. I've read the group for a couple of
> weeks and realize some personality conflicts exist - it *is* usenet
> after all.
BB is a valued member of this group and does ferment
http://en.wikipedia.org/wiki/Cruciferous_vegetables
Which leads to L. Plantarum and the FIX is in as it
takes SFB to the MAT and pins it.. LOL
http://en.wikipedia.org/wiki/Segmented_filamentous_bacteria
And once again if you take time to inspect SFB references:
Littman and Ivanov and Honda are to be found.
And once AGAIN, Lactobacillus Plantarum EATs the SFB and lowers:
Th17 which lowers IL17 which lowers TNF (the object of tNF blockers)
and thus your topical maniFESTations.. LOL
And it works.
Thank you.. very mush!
And the reverse as you've so aptly stated to jxr (JRstern) your
worried about
your immunity.
which is predicated upon a strong TNF response.
Hence the SFB in your small intestine is KEY.
Or homeostatic at the Least, to prevent CANCER (a T helper 2 cell
skew).
>
>
>
> > I will start my OWN group and then use links to THESE LONG posts chock
> > a block
> > full of pubmed ABSTRACTS....
>
> > Which... IMO... science DOES matter... (<G><w>)
>
> >http://en.wikipedia.org/wiki/NNTP
> >http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
>
> > And will bohgosity cop to which of these he's using?
> >http://en.wikipedia.org/wiki/Comparison_of_Usenet_newsreaders
>
> Why/how would that matter? How does "view profile" relate to me in
> usenet?
Those two birds being computer savvy while the afflictee or me being
able to drive but unwilling to go under the hood so to speak in this
metaphorical arena.
So if i know BB's feed i can duplicate his situation and prevent it?
But, please, never MIND.. i'll figure it out at some point in TIME.
or not?
>
>
>
> > So we know how this works?
>
> How *what* works?
>
>
>
> > Maybe FromtheRAFTERs can tell us or me?
>
> I'd probably try if I knew what you were going on about.
It's like me trying to learn something i've not got any interest in or
care FOR? LOL
Is that simple enough?
I could give a flying fig computer wise how they WORK.
I only want to get good performance on the ROAD and not worry as to
the workings of the engine etc.
Yet if man and computer have a future in the near FUTURE.. or
metaphorical marriage
if you will.
Then i might FAN the flames of my desire?
Saw Jeff Hawkins on UCSD tv today.
So went and found it online/youtube.
On Intelligence with Jeff Hawkins - Conversations with History
http://www.youtube.com/watch?v=e5xyF84dw2o
<59:24> <781 views>
Published on Nov 29, 2012
(Visit: http://www.uctv.tv/) Conversations host Harry Kreisler
welcomes Jeff Hawkins, founder of both Palm Computing and Handspring
and creator of the Redwood Neuroscience Institute, to promote research
on memory and cognition. Hawkins traces his intellectual journey
focusing on his lifelong passion to develop a theory of the brain.
Hawkins explicates the brain's operating principles and explores the
implications of human intelligence for engineering intelligent
machines, the goal of his new company Numenta. Series: "Conversations
with History" [12/2012] [Science] [Show ID: 24454]
<snip>
The gist is neo cortex and robotics i think? or iirc!
And since having a functional cortex is a GOOD idea... i may go more
digital?
If you get my drift?
http://en.wikipedia.org/wiki/Neocortex
Then AGAIN:
http://www.huffingtonpost.com/paul-raeburn/proof-of-heaven-bestseller-lists_b_2193497.html
Proof of Heaven, Neurosurgeon's Mystical Revelation, Climbs the
Bestseller Lists
[...] Alexander has made much of the supposed "fact" that his "entire
neocortex -- the outer surface of the brain, the part that makes us
human -- was entirely shut down, inoperative." Dr. Martin Samuels,
chairman of the neurology department at Brigham and Women's Hospital,
told the Times that "there is no way to know, in fact, that his
neocortex was shut down." Samuels also dismissed the notion that
Alexander's medical background gives him some authoritative edge on
near-death experiences. "The fact that he is a neurosurgeon is no more
relevant than if he was a plumber."
<snip>
While i found Jeff Hawkins to be quite credible not entirely sure i
would stick a thingy bob
in my brain to interface the NET?
To fringe-ish sounding if you watch that friday night
this show
http://en.wikipedia.org/wiki/Fringe_(TV_series)
[...] leading Peter to lethally remove a device implanted in an
Observer's spine and insert it in himself as to become like the
Observers himself. Peter uses the abilities of the implant to plot
against Captain Windmark, while Olivia fears that she may be losing
Peter again.
<snip>
But at the LAST second Peter took the device out of this head last
night... LOL
So love and mushy stuff triumphs.
But will they GAIN BACK FREEDOM in future episodes?
well...Duh!
This isn't REAL life... now.. <g>
>
>
>
> > and RAFTER and his PPP
>
> > If/When you onset with pustular there had to BE a Trigger.
>
> > Or so we've been led to believe.
>
> Do you doubt this? For myself, I was doing nothing different from what
> I had been doing for some years when all of a sudden in early June I
> seemed to be wearing barbed-wire socks to work.
The BARB part is more fit for a shrimp perhaps?
And you might take a clue from JULIE.
As she's an expert on what does or doesn't work and to take a stab
here,
i'd say you sound more like a mixture of Th1/Th2 skews.
NOT plaque but more sebopsoriasis or two things going on
simultaneously.
So either find the BEST doctor for pustular or toss a dart at the
white pages.
>
> > So once it happens an epic-genetic event onsets that doesn't change in
> > the course of having psoriasis almost 100% of the time..
> > Unless you use TNF blocker's till the day you expire..
>
> > The trigger:
>
> > Something like antibiotics or STREP (candida et al) for instance.
>
> > Noticed - rafter --> ppp- link:
> >http://www.everydayhealth.com/psoriasis/living-with-pustular-psoriasi...
> > Unless you use TNF blocker's till the day you expire..
>
> > The trigger:
>
> > Something like antibiotics or STREP (candida et al) for instance.
>
> > Noticed - rafter --> ppp- link:
>
> Not a very uplifting story as I recall.
>
> > If it had been hpa-axis susan the game would be a FOOT. LoL
>
> > Elementary as i'm watching it.. LOL
>
> > <I was doing this last night while enjoying sherlock "elementary" and
> > cute watson [ lucy Liu])
>
> >http://www.huffingtonpost.com/2012/09/27/elementary-lucy-liu_n_191961...
> Not a very uplifting story as I recall.
>
> > If it had been hpa-axis susan the game would be a FOOT. LoL
>
> > Elementary as i'm watching it.. LOL
>
> > <I was doing this last night while enjoying sherlock "elementary" and
> > cute watson [ lucy Liu])
>
>
> ...and *now* back to our regularly scheduled program.
>
> [...]
>
> > ----------------
>
> > ok..carry on tar baby..>
>
> > Does affected skin look like this:
> >http://upload.wikimedia.org/wikipedia/en/9/91/Acute_generalized_exant...
> ...and *now* back to our regularly scheduled program.
>
> [...]
>
> > ----------------
>
> > ok..carry on tar baby..>
>
> > Does affected skin look like this:
>
> Those little raised white spots can be found on my hands, but my feet
> had larger blisters than that and they looked a lot like hamburger
> patties with toes.
>
> Thanks for the links, I'll get to the rest of them later as I can't sit
> for long. It seems like the blood pressure hurts my feet when I'm
> sitting or standing.
>
> [...]
OK..as the REST of it simply points at the FACTs...
> Those little raised white spots can be found on my hands, but my feet
> had larger blisters than that and they looked a lot like hamburger
> patties with toes.
>
> Thanks for the links, I'll get to the rest of them later as I can't sit
> for long. It seems like the blood pressure hurts my feet when I'm
> sitting or standing.
>
> [...]
Just the FACTs..<and quite good ONEs if i must say.. LOL>
I did send an email to the card14 TEAM.
To see if they AGREE whether it's a mutation of card14 and the likely
hood
of pustular being genetically permanent now.
IOWs you're screwed for LIFE.
Since the BOWCOCK lab has had my family DNA for a LONG time, they
might go
an extra few minutes out of their WAY to run the gene's?
Will see or i have my doctor contact them.
They treat him like a million bucks.. LOL
OH and happy HANUKKAH ... to those who observe.
randall..
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