Key molecular events in the immune system contribute to Inflammatory Bowel Disease (IBD)

Scientists at the Virginia Bioinformatics Institute at Virginia Tech have discovered some of the key molecular events in the immune system that contribute to inflammatory bowel disease.

The results, which help researchers move one step further in their efforts to develop new drugs to treat inflammatory and immune-mediated diseases, are reported in the November 2010 edition (http://www.ncbi.nlm.nih.gov/pubmed/21068720) of the journal Mucosal Immunology from the Nature Publishing Group.

Inflammatory bowel disease starts when the gut initiates an abnormal immune response to some of the one hundred trillion or so bacteria that come into contact with the colon of the human body.

More than 1 million people are affected by inflammatory bowel disease in North America alone and direct healthcare expenses for inflammatory bowel disease in the United States are estimated at more than $15 billion annually.

Earlier mathematical and computational work (http://www.ncbi.nlm.nih.gov/pubmed/20362587) by the scientists pinpointed a special type of immune cell as a possible target for intervention strategies to fight inflammation-related disease in the gut.

The immune cells identified in the earlier work, which are known as M1 or classically activated macrophages, cause inflammation and possess a specific molecule, peroxisome proliferator-activated receptor-gamma, that, when activated, favors a switch to a type of macrophage that reduces the impact of inflammation (alternatively activated macrophage or M2) .

The activation of the receptor protein and the anti-inflammatory M2 macrophage switch plays a beneficial role in reducing the severity of the disease in the gut during experimentally induced inflammatory bowel disease.

“We have been able to validate experimentally some of the key events that take place in the regulation of the mucosal immune system when inflammatory bowel disease is triggered in mice,” said Josep Bassaganya-Riera, associate professor of immunology at the Virginia Bioinformatics Institute, leader of the Nutritional Immunology and Molecular Medicine Group in the institute’s CyberInfrastructure Division, and principal investigator.

“When we produce mice that lack the peroxisome proliferator-activated receptor-gamma specifically found in macrophages, the severity of inflammatory bowel disease increases significantly. In parallel, we are able to observe the impact of the onset of disease on key inflammation-related genes and other molecules involved in inflammation and metabolism.”

More on this article here Science blog website