A team of Emory University pathologists has discovered that non-pathogenic bacteria within the gastrointestinal tract may be responsible for blocking an immune pathway that otherwise could cause an unhealthy inflammatory response to the millions of bacteria normally present in the intestine. A breakdown in this mechanism for bacterial tolerance could play a fundamental role in the pathogenesis of inflammatory bowel disease (Crohn's disease and ulcerative colitis) and other infectious intestinal diseases. The research was reported in the September 1 issue of the journal Science.
The gastrointestinal tract of humans and other vertebrates is home to a delicate bacterial balancing act in which a diverse ecosystem of non-pathogenic bacteria co-exist among potential pathogens, all under the watchful guard of protective immune cells. Although the intestinal non-pathogenic bacteria, or normal flora, are known to play a biological role in enabling the breakdown of certain vitamins and other substances, scientists have generally believed these bacteria to be otherwise inert residents of the GI tract. The usually harmonious co-existence between intestinal organisms and immune cells dates back through millions of years of evolution, from the time of the earliest known vertebrates.
The Emory team of pathologists, including Andrew Neish, M.D., James Madara, M.D. and Andrew Gewirtz, Ph.D., and their colleagues, discovered that non-pathogenic bacteria in the G.I. tract are not merely the innocent intestinal wallflowers they were presumed to be, but that they actually deliver a signal that blocks an important immune-system pathway called NF-KB -- a transcription factor involved in activating genes in the immune system.
"It's fascinating that the epithelium (lining of the intestine) can tolerate the presence of this density of bacteria while also being quite permeable to nutrients and fluids," says Dr. Neish. "Almost all other tissue types in the body are exq
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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University Health Sciences Center
31-Aug-2000