Hi. I have lurked off and on here for a few years. I have some sort of
autoimmune disorder. While I am gluten intolerant and have Celia
atrophy, the progress of my illness is not typical to celiac. I also
have symtoms of Crohns', but again the doctors say I am atypical. One
of the symtoms that they claim is abnormal to either illness is severe
and chronic pain.
The group right now is a mess. Little useful info is posted and the
info that does get posted is questionable. This is one of the reasons
I have not contributed here. I urge everyone to post information with
links to the source like I have done below.
I am interested in hearing how other's have been dealing with the
disease and the symtoms. I have been on a very strict gluten free diet
for several years, and while this has improved my health, I still am
very ill. I can become ill by slight contamination from bread crumbs
and such. Are there others here that are this sensitive?
http://www.sciencedaily.com/releases/2007/03/070314134742.htm
Researchers Identify Molecular Basis Of Inflammatory Bowel Disease
Science Daily — Inflammatory bowel diseases, such as Crohns' disease
and Ulcerative Colitis, severely impair the lives of more than four
million people worldwide. The development of effective therapies
against these diseases requires an understanding of their underlying
molecular mechanisms. Researchers from the Universities of Cologne and
Mainz in Germany, the Mouse Biology Unit of the European Molecular
Biology Laboratory (EMBL) in Italy and their collaborators, have now
deciphered a molecular signal that triggers chronic intestinal
inflammation.
The study, which is published in the current online issue of Nature,
shows that blocking a signaling molecule causes severe intestinal
inflammation in mice and reveals a molecular mechanism that is likely
to also underpin human inflammatory bowel disease.
Our gut is home to an enormous number of bacteria, which live in
harmony with us and help in food digestion. If they penetrate the wall
of the intestine, however, these bacteria can become harmful and cause
diseases. This is why a thin, continuous layer of interconnected
cells, called an epithelium, lines the intestinal surface creating a
barrier that prevents bacteria from crossing that border. The
mechanisms that control the integrity of the epithelium and contribute
to maintaining a healthy gut have remained unknown.
Arianna Nenci from the group of Manolis Pasparakis at the University
of Cologne and Christoph Becker, a member of Markus Neurath's group in
Mainz, investigated the role of NF-kB, a signaling molecule that helps
cells cope with stress, in the intestinal epithelium. Using
sophisticated genetic methods, they generated a mouse model that does
not express NEMO, a protein needed to activate NF-kB, in intestinal
epithelial cells. As a result, these mice developed severe chronic
intestinal inflammation very similar to Colitis in humans.
"A close look at the mice revealed that their gut epithelium was
damaged," says Manolis Pasparakis, who recently moved from heading a
lab at EMBL to becoming a professor at the University of Cologne.
"NF-kB acts as a survival signal for cells. Without the molecule cells
are much more likely to die and this is what happened in the
intestines of our mice; individual epithelial cells died disrupting
the gut lining."
Through these gaps bacteria could penetrate the intestinal wall. Right
behind the gut epithelium lie cells of the intestinal immune system,
the biggest immune system of our body. It detects the invading
bacteria and generates a strong immune response to fight off the
invaders. In the process of combating the bacteria, the immune cells
secrete a cocktail of signals that bring about the symptoms of
inflammation.
"This is where the vicious cycle closes," explains Markus Neurath,
professor at the University of Mainz. "Inflammatory signals also reach
the epithelial cells that due to the lack of NF-kB are very sensitive
to them and die. The death of more epithelial cells creates bigger
gaps in the gut lining so that more bacteria enter. The result is a
constant immune response leading to chronic inflammation as we know it
from inflammatory bowel diseases in humans."
The finding that defective NF-kB signaling in the gut epithelium
initiates the outbreak of inflammation in the intestine provides a new
paradigm for the pathogenesis of inflammatory bowel disease. Since the
immune systems of mice and humans are very similar, the insights
gained through the mouse model are steps towards a better
understanding of the mechanisms causing human inflammatory bowel
diseases and may pave the way for novel therapeutic approaches.
Note: This story has been adapted from a news release issued by
European Molecular Biology Laboratory.
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