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Developing More Effective Drugs to Combat Inflammatory Bowel Disease

by Dr. Trupti Shirole on December 23, 2016 at 11:47 PM
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 Developing More Effective Drugs to Combat Inflammatory Bowel Disease

An inflammatory molecule called Tumor Necrosis Factor Alpha (TNF-alpha) is a protein produced by the body's cells. It signals other cells that then produce additional inflammatory factors.

Previous research suggests that TNF-alpha also induces specialized immune surveillance cells, called M cells, which both promote inflammation and suppress it. In other words, TNF-alpha plays a role in the destruction and the healing of tissues - a double-edged sword.

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A valuable tip that could help make more effective drugs that block TNF-alpha has been offered by a new research by a team of biomedical scientists at the University of California, Riverside, led by David Lo.

Inflammatory bowel disease is a chronic inflammatory disease of the intestine that includes Crohn's disease and ulcerative colitis. It is commonly treated with one of several available biological drugs that block TNF-alpha, but not everybody is helped by this treatment.
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"M cells normally help the immune system detect microbes in the gut, but in the case of IBD, these may also help bacteria enter tissues and worsen the inflammation," explained Lo, a distinguished professor of biomedical sciences in the School of Medicine. His lab now reports that that while there are two receptors for TNF-alpha, only one receptor, TNFR2, induces M cells. Currently, TNF-alpha-targeted drugs block both TNFR1 and TNFR2.

"Newer therapies might be more effective by targeting only TNFR2," Lo said. "As an analogy, if a soldier knew her enemy was hiding in one of two caves, she would not debate which cave she should target; she might blow up both. But if she knows her enemy is in Cave A, then why would she waste ammunition and risk innocent bystanders by attacking Cave B as well?"

Study results appear online in the Journal of Crohn's and Colitis.

The body's intestinal lining has epithelial cells that form a barrier so that bacteria in the gut do not pass on into the rest of the body. During inflammation that occurs in IBD infection, TNF-alpha triggers an increase in the number of M cells along the colon. The M cells act like selective gates and serve as a conduit for pathogens to get across the barrier and into the body.

"The question is if you have more M cells, do you have better immune surveillance or do you have more bacteria getting across the barrier?" Lo said. "From a therapeutic point of view we might want to tamp M-cell production down just enough so that the immune system can do its job without having a whole lot of bacteria pass into the body from inside the gut."

Lo explained why not everybody with IBD benefits from anti-TNF drugs.

"These drugs target both TNRF-alpha receptors: TNFR1 and TNFR2," he said. "But our research identifies a distinct inflammation-inducible M-cell population that is dependent on TNFR2 signaling, but not TNFR1. If too many M cells are being produced, then the anti-TNF drug being used is not sufficiently blocking TNRF2, which induces the M cells, and is instead blocking the other receptor. If we understand why there are two receptors, then instead of drugs doing a global blockade, more focused therapeutic approaches could target only one of the receptors, resulting in a more efficient suppression of the inflammation we see in IBD."

An ongoing challenge for biomedical scientists doing IBD research is gaining a full understanding of the role M cells play in chronic inflammation. It remains unclear whether M cells help promote continuing inflammation or whether they are critical to initiating immuno-regulatory mechanisms.

"Knowing these roles should lead to more specifically targeted therapies that will promote the regulation and resolution of chronic intestinal inflammation," Lo said.

Source: Eurekalert
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