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New NIH grants to develop Patient-Reported Outcomes Measurement Information System

October 11, 2017

In the same way, commensal microbes-beneficial bacteria-could decrease our susceptibility to various pathogenic invaders. "So you can immediately see some practical application of this, if one can mimic the presence of these commensal bacteria to strengthen resistance to pathogenic microbes," Dr. Littman says.

Thanks to rapid progress in the field of genomics, he expects the entire DNA sequence of the SFB species to be completed within a few months. Armed with the sequence, researchers could focus on specific proteins. "For example, can we identify a protein that, when we inject it into an epithelial cell, sets off in motion the whole pathway to make Th17 cells?" he says. "By knowing how to do this, you may be able to give people a peptide or a compound that induces Th17 cells by mimicking the bacterial product, and in that way either protect or ameliorate the effect of the infection."

Too much Th17 cell activation, however, can lead to harmful inflammation, Dr. Littman says. Excessive induction by specific microbes in the gut, then, could contribute to autoimmune diseases such as rheumatoid arthritis, psoriasis, Crohn's disease, and possibly even multiple sclerosis.

Source: NYU Langone Medical Center / New York University School of Medicine