BOSTON, Oct. 9 (UPI) -- U.S. experiments with mice have identified an immune deficiency as the likely cause of ulcerative colitis -- a severe inflammatory disease of the colon.
Harvard School of Public Health scientists also determined that once the disease was established in mice, it could be passed from mother to offspring and even between adult animals.
The researchers said they linked ulcerative colitis in mice to a deficiency of a molecular "peacekeeper" in the immune system, allowing harmful bacteria in the large intestine to breach the bowel's protective lining and trigger damaging inflammation.
A team led by Professor Laurie Glimcher details a series of immunological events by which a shortage of a regulatory protein called T-bet opens the way to a bacterial attack on the intestinal wall. The resulting inflammation causes the characteristic colitis that's marked by open sores throughout the colon.
With its close mimicry of human ulcerative colitis, the animal model will have unprecedented value for testing new therapies and preventive measures, said Glimcher.
The study, which included research fellow Wendy Garrett and Graham Lord, now a professor at King's College in London, is posted online in the journal Cell.
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