Sarkis K. Mazmanian ---Curing Th2 (Cancer) with GUT BUGs<--- my kinda scientist. --> AS L. Plantarum (Kimchi) cures Th1 (autoimmunity conditions)
randall
Wow... do YOU see how stuPidly the stuff from the media looks?
16,000 hits for obama saying something dumb to netanyahu?
http://www.google.com/search?hl=en&biw=1655&bih=851&tbm=nws&q=obama+netanyahu
Then netaynyahu telling obama to fry some fish. LoL
Can't we talk about something mo Fo important?
YES of course...
But you just said:
May 20 2011 3:40 pm
Subject: The PSOR raPture is COMING or CAMpING? (PART I)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/db4f5243b5516c95
And part II:
May 20 2011 4:01 pm
Subject: part II -->PSOR COMING raPture isn't COMING -- ARE YOU GOing
ANYWAY?
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/5fff109cf4eeaad7
Right and while news worry a total pile of CRAP..
Like a democrap or repuglican't crap?
You mean a rino?
Whatever... it's crapazoid time. Filling up our minds with more crap
then what's in a psor cell.
see:
CD98hc or Cd95 posts
http://groups.google.com/groups/search?q=cd95++randall+psoriasis&btnG=Search&sitesearch=
http://groups.google.com/groups/search?q=cd98hc++randall+psoriasis&sitesearch=
------------------------------------
I want a CURE and i KNOW BIG PIG Pharma or uncle SAM ain't gonna do it
for me.
How do i know?
Cause i found it on my OWN. And i knew they had a vested interest in
robbing
me BLIND.
You want to come to the LIGHT or STAY Blind?
And i've dedicated my LIFE to bring it to other psor slobs like me.
But now that i did the work i found that gut flora can skew you to far
towards Th1 (Th17)
and cause autoimmunity or the oPPosite direction of Th2 (IL-10, TREGs,
Foxp3) and create cancer or hiv/aids.
How...
WELL we've got a NEW guy working FOR us... and he's RAD...
And i'm GLAD that REAL scientists are on BOARD.
Finally... i've BEEN right here waiting and there all over the PLACE
now.
YOu have 1000 trillium bacteria in you?
No, no.
We did that yesterday.
No, no, we did it on Wed, May 18 2011 1:17 pm
Subject: Trillium Gut BActeria & BEhavioural illnesses --RNF114 --
>PSORs12 -- Gut Bullets-->LAB master<--->GLENN GIBSON -->Microbiome &
Metabonomics --> Jeffrey GORDON --NM DELZENNE - GLP-2 _ Chitin Glucan
Fiber
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/569ebe9e1835ed2b
Oh i'm so old i almost forgot, good thing my id isn't an OLD squid
like 89 year old
we're ALL Gonna die on the rapture tomorrow harold Camper?
Harold... your OLD and not a camper but an EDSEL.... smoke some
medical mary jane or
do epoptes or hit bible of some american indians...peyote?
So?
I only do what i do BEST...
Find those on MY BAND wagon.. or on my radar... or on my wave lenght?
Or, or, full of a trillion GOOD gut bugs...<Wink>
The human gut is filled with 100 trillion symbiotic bacteria—ten times
more microbial cells than our own cells—representing close to one
thousand different species. "And yet, if you were to eat a piece of
chicken with just a few Salmonella, your immune system would mount a
potent inflammatory response," says Sarkis K. Mazmanian, assistant
professor of biology at the California Institute of Technology
(Caltech).
Salmonella and its pathogenic bacterial kin don't look that much
different from the legion of bacteria in our gut that we blissfully
ignore, which raises the question: What decides whether we react or
don't? Researchers have pondered this paradox for decades.
In the case of a common "friendly" gut bacterium, Bacteroides
fragilis, Mazmanian and his colleagues have figured out the surprising
answer: "The decision is not made by us," he says. "It's made by the
bacteria. Since we are their home, they hold the key to our immune
system."
What's more, the bacteria enforce their "decision" by hijacking cells
of the immune system, say Mazmanian and his colleagues, who have
figured out the mechanism by which the bacteria accomplish this feat—
and revealed an explanation for how the immune system distinguishes
between beneficial and pathogenic organisms.
In addition, the work, described in the April 21 issue of Science
Express, "suggests that it's time to reconsider how we define self
versus non-self," Mazmanian says.
Like other commensal gut bacteria—those that provide nutrients and
other benefits to their hosts, without causing harm—B. fragilis was
thought to live within the interior of the gut (the lumen), and thus
far away from the immune system. "The dogma is that the immune system
doesn't respond to symbiotic bacteria because of immunological
ignorance," Mazmanian explains. "If we can't see them, we won't react
to them."
But using a technique called whole-mount confocal microscopy to study
the intestines of mice, he and his colleagues found that the bacteria
actually live in a unique ecological niche, deep within the crypts of
the colon, "and thus in intimate contact with the gut mucosal immune
system," he says.
"The closeness of this association highlights that an active
communication is occurring between the bacteria and their host," says
Caltech postdoctoral scholar June L. Round.
From that vantage point, the bacteria are able to orchestrate control
over the immune system—and, specifically, over the behavior of immune
cells known as regulatory T cells, or Treg cells. The normal function
of Treg cells is to prevent the immune system from reacting against
our own tissues, by shutting down certain immune responses; they
therefore prevent autoimmune reactions (which, when uncontrolled, can
lead to diseases such as multiple sclerosis, type 1 diabetes, lupus,
psoriasis, and Crohn's disease).
Bacteroides fragilis has evolved to produce a molecule that tricks the
immune system into activating Treg cells in the gut, but in this case,
Mazmanian says, "the purpose is to keep the cells from attacking the
bugs. Beautiful, right?"
In their Science paper, Mazmanian and colleagues describe the entire
molecular pathway that produces this effect. It starts with the
bacteria producing a complex sugar molecule called polysaccharide A
(PSA). PSA is sensed by particular receptors, known as Toll-like
receptors, on the surfaces of Treg cells, thus activating those cells
specifically. In response, Treg cells suppress yet another type of
cell, the T helper 17 (Th17) cells. Normally, Th17 cells induce pro-
inflammatory responses—those that would result, for example, in the
elimination of foreign bacteria or other pathogens from the body. By
shutting those cells down, B. fragilis gets a free pass to colonize
the gut. "Up until now, we have thought that triggering of Toll-like
receptors resulted solely in the induction of pathways that eliminate
bacteria," says Round. "However, our studies suggest that multiple yet
undiscovered host pathways allow us to coexist with our microbial
partners."
When Mazmanian and his colleagues blocked this mechanism—by removing
the PSA molecule, by removing the Toll-like receptor for PSA, or by
eliminating the Treg cells themselves—the bacteria were attacked by
the immune system and expelled. "They can no longer co-opt the immune
system into inducing an anti-inflammatory response, so the formerly
benign bacterium now looks like a pathogen," he says, "although the
bug itself is exactly the same."
"Our immune system arose in the face of commensal colonization and
thus likely evolved specialized molecules to recognize good bacteria,"
says Round. Mazmanian suspects that genetic mutations in these
pathways could be responsible for certain types of immune disorders,
including inflammatory bowel disease: "The question is, do patients
get sick because they are rejecting bacteria they shouldn't reject?"
On a more philosophical level, Mazmanian says, the findings suggest
that our concept of "self" should be broadened to include our many
trillions of microbial residents. "These bacteria live inside us for
our entire lives, and they've evolved to look and act like us, as part
of us," he says. "As far as our immune system is concerned, the
molecules made by gut bacteria should be tolerated similarly to our
own molecules. Except in this case, the bacteria 'teaches' us to
tolerate them, for both our benefit and theirs."
###
The other coauthors on the paper, "The Toll-like receptor 2 pathway
establishes colonization by a commensal of the human microbiota," are
S. Melanie Lee, Jennifer Li, and Gloria Tran of Caltech; Bana Jabri of
the University of Chicago; and Talal A. Chatila of the David Geffen
School of Medicine at UCLA. June L. Round was supported by a Jane
Coffin Childs Memorial Fund postdoctoral fellowship. The work was
supported by the National Institutes of Health, the Damon Runyon
Cancer Research Foundation, and the Crohn's and Colitis Foundation of
America.
Written by Kathy Svitil
--------------------------------------
Sarkis K. Mazmanian
http://biology.caltech.edu/Members/Mazmanian
[...] http://biology.caltech.edu/Members/Mazmanian/Symbiotic.jpeg
Symbiotic bacteria elaborate immunomodulatory molecules which are
recognized by host immune cells (dendritic cells), and presented to T
cells in order to mediate development of the mammalian immune system.
<snip>
-------------
Sarkis has a youtube:
Sarkis K. Mazmanian, PhD, Damon Runyon Scientist
http://www.youtube.com/watch?v=IGQGwwXfXeU
Dr. Mazmanian's hypothesis is that intestinal bacteria are a critical
factor in cancer. He proposes that these bacteria have evolved ways to
protect their hosts us from diseases. Furthermore, societal and
medical changes of the past few decades (antibiotics, sanitation,
vaccination, diet, hygiene) have disturbed our association with these
"good" bacteria, potentially leading to cancer. He hopes that better
understanding of the relationship between intestinal bacteria and our
immune systems may lead to new natural therapeutics for colon cancer.
Learn more about Sarkis and meet more of today's brightest minds in
cancer research at http://www.damonrunyon.org
<snip>
Hey, mazmanian might only be 35 years old but he's light years ahead
of oldsters who could give a fig about your gut and cancer.
LOL
Let's see, i've mentioned him over 10 times on the P NG
http://groups.google.com/groups/search?hl=en&qt_s=1&q=mazmanian+randall+psoriasis
And "Mazmanian SK"[Author]--> has 31 hits -pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mazmanian%20SK%22%5BAuthor%5D
#1 of the 31:
http://www.ncbi.nlm.nih.gov/pubmed/21512004
Science. 2011 Apr 21.
The Toll-Like Receptor 2 Pathway Establishes Colonization by a
Commensal of the Human Microbiota.
Round JL, Lee SM, Li J, Tran G, Jabri B, Chatila TA, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena, CA
91125, USA.
Abstract
Mucosal surfaces constantly encounter microbes. Toll-like receptors
(TLRs) mediate recognition of microbial patterns to eliminate
pathogens. In contrast, we demonstrate that the prominent gut
commensal, Bacteroides fragilis, activates the TLR pathway to
establish host-microbial symbiosis. TLR2 on CD4+ T cells is required
for B. fragilis colonization of a unique mucosal niche in mice during
homeostasis. A symbiosis factor (PSA) of B. fragilis signals through
TLR2 directly on Foxp3+ regulatory T cells to promote immunologic
tolerance. Remarkably, B. fragilis lacking PSA is unable to restrain T
helper 17 (Th17) responses and is defective in niche-specific mucosal
colonization. Therefore, commensal bacteria exploit the TLR pathway to
actively suppress immunity. We propose that the immune system can
discriminate between pathogens and the microbiota via recognition of
symbiotic bacterial molecules in a process that engenders commensal
colonization.
PMID: 21512004
#2 of the 31
http://www.ncbi.nlm.nih.gov/pubmed/21205662
Science. 2010 Dec 24;330(6012):1768-73.
Has the microbiota played a critical role in the evolution of the
adaptive immune system?
Lee YK, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena, CA
91125, USA.
Abstract
Although microbes have been classically viewed as pathogens, it is now
well established that the majority of host-bacterial interactions are
symbiotic. During development and into adulthood, gut bacteria shape
the tissues, cells, and molecular profile of our gastrointestinal
immune system. This partnership, forged over many millennia of
coevolution, is based on a molecular exchange involving bacterial
signals that are recognized by host receptors to mediate beneficial
outcomes for both microbes and humans. We explore how specific aspects
of the adaptive immune system are influenced by intestinal commensal
bacteria. Understanding the molecular mechanisms that mediate
symbiosis between commensal bacteria and humans may redefine how we
view the evolution of adaptive immunity and consequently how we
approach the treatment of numerous immunologic disorders.
PMID: 21205662
#5 of the 31:
http://www.ncbi.nlm.nih.gov/pubmed/20566854
Proc Natl Acad Sci U S A. 2010 Jul 6;107(27):12204-9. Epub 2010 Jun
21.
Inducible Foxp3+ regulatory T-cell development by a commensal
bacterium of the intestinal microbiota.
Round JL, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena, CA
91125, USA.
Abstract
To maintain intestinal health, the immune system must faithfully
respond to antigens from pathogenic microbes while limiting reactions
to self-molecules. The gastrointestinal tract represents a unique
challenge to the immune system, as it is permanently colonized by a
diverse amalgam of bacterial phylotypes producing multitudes of
foreign microbial products. Evidence from human and animal studies
indicates that inflammatory bowel disease results from uncontrolled
inflammation to the intestinal microbiota. However, molecular
mechanisms that actively promote mucosal tolerance to the microbiota
remain unknown. We report herein that a prominent human commensal,
Bacteroides fragilis, directs the development of Foxp3(+) regulatory T
cells (Tregs) with a unique "inducible" genetic signature.
Monocolonization of germ-free animals with B. fragilis increases the
suppressive capacity of Tregs and induces anti-inflammatory cytokine
production exclusively from Foxp3(+) T cells in the gut. We show that
the immunomodulatory molecule, polysaccharide A (PSA), of B. fragilis
mediates the conversion of CD4(+) T cells into Foxp3(+) Treg cells
that produce IL-10 during commensal colonization. Functional Foxp3(+)
Treg cells are also produced by PSA during intestinal inflammation,
and Toll-like receptor 2 signaling is required for both Treg induction
and IL-10 expression. Most significantly, we show that PSA is not only
able to prevent, but also cure experimental colitis in animals. Our
results therefore demonstrate that B. fragilis co-opts the Treg
lineage differentiation pathway in the gut to actively induce mucosal
tolerance.
Comment in
Nat Rev Microbiol. 2010 Aug;8(8):534.
Nat Rev Immunol. 2010 Aug;10(8):539.
PMID: 20566854
PMCID: PMC2901479
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20566854/?tool=pubmed
#3 of 31
http://www.ncbi.nlm.nih.gov/pubmed/21034976
Adv Immunol. 2010;107:243-74.
Host-bacterial symbiosis in health and disease.
Chow J, Lee SM, Shen Y, Khosravi A, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena,
California, USA.
Abstract
All animals live in symbiosis. Shaped by eons of co-evolution, host-
bacterial associations have developed into prosperous relationships
creating mechanisms for mutual benefits to both microbe and host. No
better example exists in biology than the astounding numbers of
bacteria harbored by the lower gastrointestinal tract of mammals. The
mammalian gut represents a complex ecosystem consisting of an
extraordinary number of resident commensal bacteria existing in
homeostasis with the host's immune system. Most impressive about this
relationship may be the concept that the host not only tolerates, but
has evolved to require colonization by beneficial microorganisms,
known as commensals, for various aspects of immune development and
function. The microbiota provides critical signals that promote
maturation of immune cells and tissues, leading to protection from
infections by pathogens. Gut bacteria also appear to contribute to non-
infectious immune disorders such as inflammatory bowel disease and
autoimmunity. How the microbiota influences host immune responses is
an active area of research with important implications for human
health. This review synthesizes emerging findings and concepts that
describe the mutualism between the microbiota and mammals,
specifically emphasizing the role of gut bacteria in shaping an immune
response that mediates the balance between health and disease.
Unlocking how beneficial bacteria affect the development of the immune
system may lead to novel and natural therapies based on harnessing the
immunomodulatory properties of the microbiota.
PMID: 21034976
#4 of 31
http://www.ncbi.nlm.nih.gov/pubmed/20660719
Proc Natl Acad Sci U S A. 2011 Mar 15;108 Suppl 1:4615-22. Epub 2010
Jul 26.
Proinflammatory T-cell responses to gut microbiota promote
experimental autoimmune encephalomyelitis.
Lee YK, Menezes JS, Umesaki Y, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena, CA
91125, USA.
Abstract
Although the effects of commensal bacteria on intestinal immune
development seem to be profound, it remains speculative whether the
gut microbiota influences extraintestinal biological functions.
Multiple sclerosis (MS) is a devastating autoimmune disease leading to
progressive deterioration of neurological function. Although the cause
of MS is unknown, microorganisms seem to be important for the onset
and/or progression of disease. However, it is unclear how microbial
colonization, either symbiotic or infectious, affects autoimmunity.
Herein, we investigate a role for the microbiota during the induction
of experimental autoimmune encephalomyelitis (EAE), an animal model
for MS. Mice maintained under germ-free conditions develop
significantly attenuated EAE compared with conventionally colonized
mice. Germ-free animals, induced for EAE, produce lower levels of the
proinflammatory cytokines IFN-γ and IL-17A in both the intestine and
spinal cord but display a reciprocal increase in CD4(+)CD25(+)Foxp3(+)
regulatory T cells (Tregs). Mechanistically, we show that gut
dendritic cells from germ-free animals are reduced in the ability to
stimulate proinflammatory T cell responses. Intestinal colonization
with segmented filamentous bacteria (SFB) is known to promote IL-17
production in the gut; here, we show that SFBs also induced IL-17A-
producing CD4(+) T cells (Th17) in the CNS. Remarkably, germ-free
animals harboring SFBs alone developed EAE, showing that gut bacteria
can affect neurologic inflammation. These findings reveal that the
intestinal microbiota profoundly impacts the balance between pro- and
antiinflammatory immune responses during EAE and suggest that
modulation of gut bacteria may provide therapeutic targets for
extraintestinal inflammatory diseases such as MS.
PMID: 20660719
=========================
So mazmanian is kewl but not on the ultimate study (Th17 inducted by
SFB) with Ivanov and Littman and kenya Honda:
http://www.cell.com/abstract/S0092-8674(09)01248-3
But to his mazmaniac attitude towards gut bugs, to cure cancer, he did
this next one nine months before
the October (2009) study above with ivanova, littman and honda.
http://www.ncbi.nlm.nih.gov/pubmed/19154983
Cell Host Microbe. 2009 Jan 22;5(1):8-12.
Getting the bugs out of the immune system: do bacterial microbiota
"fix" intestinal T cell responses?
Chow J, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena, CA
91125, USA.
Abstract
Proinflammatory T helper 17 (Th17) cells control infections caused by
microbial pathogens. Surprisingly, several recent reports now reveal
that symbiotic gut bacteria modulate Th17 cell differentiation and
function in the gastrointestinal tract. As various autoimmune and
allergic disorders are mediated by uncontrolled T cell responses,
immune regulation by the microbiota may have direct implications for
human health.
PMID: 19154983
And he's going in the enterotypes direction no doubt.
SO he is a mazmaniac and MY kinda Doc....the FIX is in YOUR GUTz...
But enterotypage isn't a BIG DEAL or is it?
Blah blah you have three types. <w>
That is so like dirt..
It's either alkaline, acidic or somewhere between.
DUH..
And if you have an alkaline colon your dirt is forked up.
And you've got SFB in your ileum then and SFB bugging your lamina
propria going back uPstream.
So?
What do you DO?
You simply re-build the colon flora with LAB (lactic acid bacteria).
I call it re-colon-i=zation.
WELL, swell a few times anyway:
http://groups.google.com/groups/search?hl=en&q=colon-i-+zation+psoriasis&btnG=Search&sitesearch=
You won't see GOD or have the raPture unless harold camping is RIGHT
tomorrow. but you will
see your psoriasis go back towards zero.
And if you DO it yourself on a rigid diet for one month to re grow
those lactic acid loving bacteria you'll FELL like a HERO.
So get it ON.
randall...