Impunity from Autoimmunity? Lower Th17 levels due to SFB's!
randall
Did I previously post the Dan Littman abstract for SFB's in the ileum
and persistent
levels of Th17 (Th-17)?
I know i posted quite a few pieces in regards to it.
Maybe some of us JUST need less SFB in our Gi tracts?
Maybe that's why i'm nearly clear NOW and i don't take any bio ill
logicals.
A hammer will drive a nail WELL, but not in to your head. LOL
www.ncbi.nlm.nih.gov/pubmed/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.
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.
The gastrointestinal tract of mammals is inhabited by hundreds of
distinct species of commensal microorganisms that exist in a
mutualistic relationship with the host. How commensal microbiota
influence the host immune system is poorly understood. We show here
that colonization of the small intestine of mice with a single
commensal microbe, segmented filamentous bacterium (SFB), is
sufficient to induce the appearance of CD4(+) T helper cells that
produce IL-17 and IL-22 (Th17 cells) in the lamina propria. SFB adhere
tightly to the surface of epithelial cells in the terminal ileum of
mice with Th17 cells but are absent from mice that have few Th17
cells. Colonization with SFB was correlated with increased expression
of genes associated with inflammation and antimicrobial defenses and
resulted in enhanced resistance to the intestinal pathogen Citrobacter
rodentium. Thus, manipulation of this commensal-regulated pathway may
provide new opportunities for enhancing mucosal immunity and treating
autoimmune disease.
PMID: 19836068
Have I ever discussed the lamina propria?
Sounds familiar?
Let's see:::
OH MY! 80 hits for ME + lamina propria in our group::
http://groups.google.com/groups/search?hl=en&ie=UTF-8&q=psoriasis+randall+lamina+propria&sitesearch=groups.google.com
And while lamina propria and LPS are always on my radar we've now
got the AREA in the Gi tract, and it's not area 51 anymore, to observe
and
TREAT.
Do you think for one minute i'm not going to work this angle?
Do I have the energy?
LOL
www.ncbi.nlm.nih.gov/pubmed/18716618
ATP drives lamina propria T(H)17 cell differentiation.
Atarashi K, Nishimura J, Shima T, Umesaki Y, Yamamoto M, Onoue M,
Yagita H, Ishii N, Evans R, Honda K, Takeda K.
Laboratory of Immune Regulation, Graduate School of Medicine, Osaka
University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Comment in:
Gastroenterology. 2009 Mar;136(3):1107-9.
Interleukin (IL)-17-producing CD4(+) T lymphocytes (T(H)17 cells)
constitute a subset of T-helper cells involved in host defence and
several immune disorders. An intriguing feature of T(H)17 cells is
their selective and constitutive presence in the intestinal lamina
propria. Here we show that adenosine 5'-triphosphate (ATP) that can be
derived from commensal bacteria activates a unique subset of lamina
propria cells, CD70(high)CD11c(low) cells, leading to the
differentiation of T(H)17 cells. Germ-free mice exhibit much lower
concentrations of luminal ATP, accompanied by fewer lamina propria T(H)
17 cells, compared to specific-pathogen-free mice. Systemic or rectal
administration of ATP into these germ-free mice results in a marked
increase in the number of lamina propria T(H)17 cells. A CD70(high)
CD11c(low) subset of the lamina propria cells expresses T(H)17-prone
molecules, such as IL-6, IL-23p19 and transforming-growth-factor-beta-
activating integrin-alphaV and -beta8, in response to ATP stimulation,
and preferentially induces T(H)17 differentiation of co-cultured naive
CD4(+) T cells. The critical role of ATP is further underscored by the
observation that administration of ATP exacerbates a T-cell-mediated
colitis model with enhanced T(H)17 differentiation. These observations
highlight the importance of commensal bacteria and ATP for T(H)17
differentiation in health and disease, and offer an explanation of why
T(H)17 cells specifically present in the intestinal lamina propria.
PMID: 18716618
This one above was examined here: [on this group]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/4ce10d887535e2c7
Tues, Oct 28 2008 3:05 pm
Subject: SWEET WHEY Makes CENTs OR Whats uP with CD70?
Go a little over half way down the page:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/9edd45085f3c0/4ce10d887535e2c7?hl=en&lnk=gst&q=PMID%3A+18716618+%5B#4ce10d887535e2c7
===================
Lawsuits for bio ill logicals:::
You want brain cancer? Turn off your IFN and TNF levels. Yikes...
http://www.aboutlawsuits.com/brain-infection-cases-linked-tysabri-rituxan-6598/
Additional PML Brain Infection Cases Linked to Tysabri and Rituxan
New cases of a rare brain infection, progressive multifocal
leukoencephalopathy (PML), have been liked to the lymphoma and
arthritis drug Rituxan and the multiple sclerosis (MS) drug Tysabri.
The cases have regulators in the U.S. and Europe searching for ways to
reduce the risks of patients developing the often fatal brain
infection.
[...]
In April 2009, reports of PML brain infections resulted in a recall of
Raptiva, a once-weekly injection that was prescribed to treat
psoriasis. Following four brain infection reports, the FDA and
Genentech, which also manufactured Raptiva, determined that the
potentially life-threatening risk of progressive multifocal
leukoencephalopathy outweighed the benefits provided by that
medication.
Tags: Biogen, Brain Infection, Genentech, Progressive Multifocal
Leukoencephalopathy (PML), Raptiva, Rituxan, Tysabri
<sniP>
=================
IL-6 stops brain inflammation and Alzheimer's disease?
Does alzheimers make brain cancer or just stupid/fuzzy thinking?
I take a bio ill logical and die of brain cancer or grow old and
lose my MIND. YIKEs...
But what happens with chronic inflammation and IL-6?
http://www.lef.org/protocols/prtcl-146.shtml#agingandin
OK, and moving back towards homeostatic levels and exercise.
SEE:
http://www.sciencedaily.com/releases/2009/10/091022114315.htm
OR
http://news.biocompare.com/News/NewsStory/295349/NewsStory.html
STOP amyloid plaque and amyloid beta (A?) protein from making
your brain FUZZY?
Yep... get some IL-6 going and bingo...smarter brain.
Show me:
----
http://en.wikipedia.org/wiki/Interleukin_6
So?
You see and NOW go DO it.
Exercise more and build up IL-6 and look and think like
Jack LaLanne
http://en.wikipedia.org/wiki/Jack_lalanne
Jack was a student of Paul Bragg
http://en.wikipedia.org/wiki/Paul_Bragg
It's EASY to stay HEALTHY the Bragg way:
http://en.wikipedia.org/wiki/Paul_Bragg#Healthy_Lifestyle_Legacy
But if you have psoriasis or any autoimmune disease with excess
Th-17 (Th17) you need the sweet whey and wit kit implant to first
clear up the SFB in your ileum.
And then IL-6, TNF, IFN et al will go DOWN when the TREG's tell them
to.
1320 hits for keywords: randall IL-6 psoriasis
http://groups.google.com/groups/search?hl=en&q=iL-6+psoriasis+randall&btnG=Search&sitesearch=groups.google.com
-------------------
How does the mole rat avoid cancer?
http://www.sciencedaily.com/releases/2009/10/091026152812.htm
Scientists Discover Gene That 'Cancer-proofs' Naked Mole Rat's Cells
ScienceDaily (Oct. 27, 2009) — Despite a 30-year lifespan that gives
am
ple time for cells to grow cancerous, a small rodent species called a
naked mole rat has never been found with tumors of any kind -- and now
biologists at the University of Rochester think they know why.
The findings, presented in The Proceedings of the National Academy of
Sciences, show that the mole rat's cells express a gene called p16
that makes the cells "claustrophobic," stopping the cells'
proliferation when too many of them crowd together, cutting off
runaway growth before it can start. The effect of p16 is so pronounced
that when researchers mutated the cells to induce a tumor, the cells'
growth barely changed, whereas regular mouse cells became fully
cancerous.
"We think we've found the reason these mole rats don't get cancer, and
it's a bit of a surprise," says Vera Gorbunova, associate professor of
biology at the University of Rochester and lead investigator on the
discovery. "It's very early to speculate about the implications, but
if the effect of p16 can be simulated in humans we might have a way to
halt cancer before it starts."
Naked mole rats are strange, ugly, nearly hairless mouse-like
creatures that live in underground communities. Unlike any other
mammal, these communities consist of queens and workers more
reminiscent of bees than rodents. Naked mole rats can live up to 30
years, which is exceptionally long for a small rodent. Despite large
numbers of naked mole-rats under observation, there has never been a
single recorded case of a mole rat contracting cancer, says Gorbunova.
Adding to their mystery is the fact that mole rats appear to age very
little until the very end of their lives.
Over the last three years, Gorbunova and Andrei Seluanov, research
professor of biology at the University of Rochester, have worked an
unusual angle on the quest to understand cancer: Investigating rodents
from across the globe to get an idea of the similarities and
differences of how varied but closely related species deal with
cancer.
In 2006, Gorbunova discovered that telomerase -- an enzyme that can
lengthen the lives of cells, but can also increase the rate of cancer
-- is highly active in small rodents, but not in large ones.
Until Gorbunova and Seluanov's research, the prevailing wisdom had
assumed that an animal that lived as long as we humans do needed to
suppress telomerase activity to guard against cancer. Telomerase helps
cells reproduce, and cancer is essentially runaway cellular
reproduction, so an animal living for 70 years has a lot of chances
for its cells to mutate into cancer, says Gorbunova. A mouse's life
expectancy is shortened by other factors in nature, such as predation,
so it was thought the mouse could afford the slim cancer risk to
benefit from telomerase's ability to speed healing.
While the findings were a surprise, they revealed another question:
What about small animals like the common grey squirrel that live for
24 years or more? With telomerase fully active over such a long
period, why isn't cancer rampant in these creatures?
Gorbunova sought to answer that question, and in 2008 confirmed that
small-bodied rodents with long lifespans had evolved a previously
unknown anti-cancer mechanism that appears to be different from any
anticancer mechanisms employed by humans or other large mammals.
At the time she was not able to identify just what the mechanism might
be, saying: "We haven't come across this anticancer mechanism before
because it doesn't exist in the two species most often used for cancer
research: mice and humans. Mice are short-lived and humans are large-
bodied. But this mechanism appears to exist only in small, long-lived
animals."
Now, Gorbunova believes she has found the primary reason these small
animals are staying cancer-free, and it appears to be a kind of
overcrowding early-warning gene that the naked mole rat expresses in
its cells.
When Gorbunova and her team began specifically investigating mole rat
cells, they were surprised at how difficult it was to grow the cells
in the lab for study. The cells simply refused to replicate once a
certain number of them occupied a space. Other cells, such as human
cells, also cease replication when their populations become too dense,
but the mole rat cells were reaching their limit much earlier than
other animals' cells.
"Since cancer is basically runaway cell replication, we realized that
whatever was doing this was probably the same thing that prevented
cancer from ever getting started in the mole rats," says Gorbunova.
Like many animals, including humans, the mole rats have a gene called
p27 that prevents cellular overcrowding, but the mole rats use
another, earlier defense in gene p16. Cancer cells tend to find ways
around p27, but mole rats have a double barrier that a cell must
overcome before it can grow uncontrollably.
"We believe the additional layer of protection conferred by this two-
tiered contact inhibition contributes to the remarkable tumor
resistance of the naked mole rat," says Gorbunova in the PNAS paper.
Gorbunova and Seluanov are now planning to delve deeper into the mole
rat's genetics to see if their cancer resistance might be applicable
to humans.
This research was funded by the National Institutes of Health and the
Ellison Medical Foundation.
----------
P16 time again::
p16 promoter is found in psoriasis. I've posted a half a dozen or so
posts.
www.ncbi.nlm.nih.gov/pubmed/18373711
Some P16 thoughts:
p16INK4a --- P16
http://en.wikipedia.org/wiki/P16_(gene)#Clinical_significance
http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160
I see p53
Not about to read more then a few paragraphs. lol
no need with p53 your cancerous questioned is answered.
first
http://www.ncbi.nlm.nih.gov/Omim/getmap.cgi?l600160
and then
http://en.wikipedia.org/wiki/P53
====================================
Some more FLU and pig flu things to ponder:
Mercola::
http://articles.mercola.com/swine-flu-article/20091027.htm
Is there another flu treatment besides the vaccine?
http://www.lewrockwell.com/sardi/sardi129.html
[...]
In 2005 researchers in Rome, Italy wondered what backup treatment
could be used in the event vaccines were unavailable or were
ineffective against a fast mutating flu virus that had developed
resistance to vaccines or anti-viral drugs like Tamiflu or Relenza.
Flu viruses require a host cell to replicate. The Italian researchers
report that resveratrol, known as a red wine molecule, completely
blocks entry of flu viruses into the cell nucleus in animals at a
human equivalent dose of ~70 milligrams. [Journal Infectious Disease
2005 May 15; 191(10):1719–29] So the virus would enter the lungs,
antibodies would still be generated to produce long-term immunity, but
the virus could not duplicate into millions of daughter virions as it
normally does. Resveratrol works on closing the cellular doorway
rather than destroying the virus itself. Therefore it is a totally non-
toxic approach to control of influenza viruses. Furthermore,
resveratrol does not provoke viral resistance.
In contrast, anti-viral drugs like oseltamivir (Tamiflu) allow viruses
to enter cellular machinery to produce copies of the flu virus and
then inhibits their exit from the cell via inhibition of the enzyme
neuraminidase. So host cells are flooded with copies of the virus.
This approach is not ideal as it can lead to drug-induced side effects
which have been widely reported.
<sniP>
OMG-- the swine flu cure via red wine. LOL
========================
Let's build on all of the above topics?
Sure... my gray cells are cooking.
Is there a virus that makes people FAT (obese)?
Maybe...
If some funky gut bug like SFB (segmented filamentous bacterium) can
make people have
autoimmune problems related to hyper levels of Th17 then certainly a
VIRUS can make you FAT.
Why NOT?
JRstern is right.
But why wait if you can correct the problem and be part of the cURE?
I want to help our president in this regard.
What will the effects be in the future regardless of nationalized
healthcare for an autoimmune cure that we CAUSE to haPPen?
It will sAVE money regardless of what plan or lack of a plan is out
there.
And why not make FAT (Obese) psoriatics skinny in the process?
First off, is there a FAT virus?
http://junkfoodscience.blogspot.com/2009/02/obesity-virus-new-risk-factor.html
[...]
Human link to a “fat virus?”
The only published study to date linking the “fat virus,” Ad-36, to
people was first described and presented as an abstract to IASO
members in 1998, entitled “Evidence for an association of an obesity
virus with human obesity at three sites in the United
States.” [International J Obesity 1998; 22: S57 (unavailable to
nonmembers)]
This study remains the only study of Ad-36 in humans and is the study
being used to support the entire promotion of the human “obesity
virus” and the antibody tests for it. This study wasn’t published
until March, 2005 — and a lot happened in the interim. But before we
get to that, let’s briefly look at this study.
Published in the International Journal of Obesity, it reported that
“Ad-36 is associated with increased body weight and lower serum lipids
in humans.” In brief, they selected 360 “massively obese” people who
were dieting and enrolled in weight loss programs at clinics in New
York, Florida and Wisconsin; and 142 lean people recruited from the
University and area communities from 1995 to 1999. Among these groups,
11% of the lean people tested positive for the virus and 30% of the
obese dieters tested positive.
Testing for Ad-36 antibodies, along with fasting blood lipids, they
reported:
a correlation between positive antibodies for the virus and higher
BMIs: Those testing negative had average BMIs of 35.8 ±12.3 (standard
deviation) and those testing positive had average BMIs of 44.9 ±16.3
(SD).
a correlation between positive antibodies for this virus and lower
total cholesterol levels, and triglycerides: Those testing negative
had average total cholesterol levels of 5.5.1 ±0.07 (standard error)
and those testing positive had average total cholesterol levels of
4.64 ±0.11 (SE).
Did you catch the fallacies and why this wasn’t a “fair test” to
conclude the adenovirus was responsible for weight differences?
Regular readers will recognize the most glaring ones, such as
nonrandomized samples and ‘correlations aren’t causation’, but even
these correlations were questionable.
The authors compared two very different groups of people, yet made no
attempt to control for any confounding factor other than age. None.
The weak correlations were made meaningless. They only looked at one
correlation and could have chosen hundreds of other things to compare
a group of younger university students and area adults, and a group of
older, extremely ‘obese’ people undergoing weight loss interventions
at medical centers. It’s easy to come up with countless clinically
contradicting or meaningless correlations.
<sniP>
Another long version of this for the layman:
http://curezone.com/forums/fm.asp?i=586478
http://en.wikipedia.org/wiki/Adenovirus_serotype_36
This site may deal with the topic more succinctly?
http://knol.google.com/k/john-vickery/obesity-virus/3r3wsiy0fpdo3/2#
[...]
Future Research
Because of the fact that a virus can contribute to obesity, there may
well be a place for the development of an obesity vaccine. Whether or
not this vaccine would be worth the expense and any possible side
effects would depend on how effective the vaccine would be, how
strongly obesity viruses affect one's body fat, and how prevalent
these viruses are in the general population. In the meantime, the work
done on the discovery of these viruses, how they lead to being
overweight, and how they improve cholesterol profiles gives scientists
more information to guide them in developing treatments for obesity
and high cholesterol. Even though body weight is best managed by
living a healthy lifestyle consisting of diet and exercise, the more
we understand this process, the closer we come to additional therapies
to combat the obesity epidemic.
References
<sniP>
It has been my personal satisfaction to FIND one supplement that
really works with
my sweet whey daily supplement (taken with a shake or coffee or water
or you name it. lol)
And that supplement is www.longevinex.com
This resveratrol pill WORKs.
It became a lot easier to maintain MILD levels of psoriasis and still
exPand my dietary
restrictions previously on my NO NO list.
IOWs i can and DO stay clearer and eat with more impunity. Foods that
previously FLARED and
contributed the continual spreading of psoriasis DON'T.
Like a miracle, i feel nearly normal.
Now i want to go beyond this miracle to a CURE for all psoriatics and
those whose Th17 levels
lead to gut and arthritis conditions that disable and cause misery.
Can you help?
====================
randall... Love it. Impunity from Autoimmunity-- block SFB & lower
Th17 levels
manfred
> <sniP>
>
> It has been my personal satisfaction to FIND one supplement that
> really works with
> my sweet whey daily supplement (taken with a shake or coffee or water
> or you name it. lol)
>
>
Dr. David Williams "wheys" in:
<snip>
"The good news is there’s a nutrient called
XP-828L that’s derived from a natural substance found in whey protein
that modulates the immune response and reduces the occurrence of itchy
skin. IFS Defense combines XP-828L with a special form of turmeric,
one of my all-time favorites for promoting a normal inflammatory
response."
<snip>
zzznot
news:f2dd3a58-c2f6-4d3c...@m7g2000prd.googlegroups.com...
>If some funky gut bug like SFB (segmented filamentous bacterium) can
>make people have
>autoimmune problems related to hyper levels of Th17 then certainly a
>VIRUS can make you FAT.
>
>
>Why NOT?
>
>JRstern is right.
Excellent! About what - did I say anything about a fat virus?
I don't always listen to the words coming out of my keyboard ...
>It has been my personal satisfaction to FIND one supplement that
>really works with
>my sweet whey daily supplement (taken with a shake or coffee or water
>or you name it. lol)
>
>And that supplement is www.longevinex.com
>
>This resveratrol pill WORKs.
>
>It became a lot easier to maintain MILD levels of psoriasis and still
>exPand my dietary
>restrictions previously on my NO NO list.
My cousin is in some MLM scheme selling a resveratrol pill
or elixer or something ... mebbe I should try it. I'm mildly
skeptical about major differences between the many and various
bioflavinoids besides dosage, but it shouldn't hurt anything.
J.
randall
> "randall" <ranhu...@aol.com> wrote in message
J,
I'm in contact with Littman to design a trial of Th17 & SFB.
So, i'm not real excited about saying anything JUST YET.
If he doesn't want to get involved big deal, it won't stop me.
I spoke with Daid Webster (wit kit creator) at length yesterday
and feel that my previous results already prove the outcome of this
trial.
So?
If you want to take my resveratrol formula, www.longevinex.com
I'm excited and hope you have half the results i did, as it will
lead you to bigger and better trials. :)
randall.... i want to support our president & cure Ai... :)
JRStern
wrote:
>randall.... i want to support our president & cure Ai... :)
American Idol?
Artificial Intelligence?
J.