We've long known that our gut plays a role in autoimmunity. Previously, we looked at the connections between gut and brain inflammation, chronic fatigue, and rheumatoid arthritis. This week, we'll look at an autoimmune condition of the digestive lining—inflammatory bowel disease (IBD).
IBD is characterized by chronic inflammation in the gastrointestinal (GI) tract and is estimated to affect 3 million U.S. adults. Two autoimmune diseases, ulcerative colitis and Crohn's disease, fall under the umbrella of IBD. Current treatments aim to reduce symptoms and consist of corticosteroids, immunosuppressants, and biologics, which are also widely used for other autoimmune diseases.
Yet, an estimated 40% of IBD patients report not benefitting from their existing treatments. Recently, researchers at Johns Hopkins identified a gut enzyme that offers a promising new treatment.
The researchers found that a particular enzyme, called gastrointestinal glutamate carboxypeptidase II (GCPII), is overactive in patients with IBD. A 2016 study found the enzyme's activity to be 41 times greater in patients with IBD than those without.
Based on that, researchers have developed a GCPII inhibitor in hopes that it would reduce IBD symptoms. When tested on mouse models of colitis, the inhibitor was found to reduce approximately 75% of GCPII activity, resulting in improved stool consistency, decreased inflammation, and less bleeding. The GCPII inhibitor also holds promise since it was designed to be gut-restricted; that is, when taken orally, the drug primarily remains within the GI tract, ensuring minimal exposure to the rest of the body.
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