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The discovery has already launched an examination of how the protein TLR1 is linked to inflammatory bowel disease, says R. William DePaolo, assistant professor of molecular microbiology and immunology at the Keck School of Medicine of University of Southern California (USC).

“It’s not clear what drives the body’s immune response,” says DePaolo, the study’s lead investigator. “This paper identifies a receptor that is important in driving a mucosal immune response against Yersinia enterocolitica, bacteria like Salmonella and E. coli that can cause food poisoning.

“Although the receptor’s role against other bacteria is still unknown, our research emphasizes that the way the body initiates an immune response depends on the pathogen and the route of infection.”

The study is scheduled to appear in the July 30 edition of The Journal of Experimental Medicine.

DePaolo’s team compared the immune responses of mice bred with and without TLR1 when infected with Y. enterocolitica by mouth and by blood. The team found that TLR1 played a significant role in controlling mucosal infection (by mouth) but not systemic infection (by blood), initiating the creation of antibodies that specifically fight against oral infections.

“Now that we have identified the receptor’s role, the next step is to determine how we can manipulate that receptor to enhance vaccine development,” DePaolo says.

“We also are studying the receptor in different models of mucosal inflammation, including inflammatory bowel disease and colitis-associated cancers. The idea is to take a personalized approach to medicine and use genetic profiling to better treat or manage disease.”

Investigators from University of Chicago and Midwestern University also contributed to the research, which was supported by the National Institute of Diabetes and Digestive and Kidney Diseases and the Crohn’s and Colitis Foundation of America.

More news from USC: http://uscnews.usc.edu/