Common stomach bug may help cause Crohn’s disease, study finds

An illustration of norovirus particles.

An illustration of norovirus particles.
Drawing: Shutterstock (Shutterstock)

A nasty but short-lived stomach bug can have lingering consequences for a few unlucky ones. The researchers found evidence in mice and human cells that norovirus infection can trigger Crohn’s disease in people who are already genetically predisposed. The findings could also help scientists one day find better treatments for chronic bowel disease.

Crohn’s disease is one of two main types of inflammatory bowel disease. In Crohn’s disease, this inflammation occurs along the lining of the digestive tract, most often in the small intestine. Symptoms can vary greatly in severity, but often include diarrhea, weight loss, and severe stomach cramps. Affected individuals also tend to experience disease flares, with symptoms returning or worsening. About 3 million Americans are thought have IBD.

The underlying mechanism behind Crohn’s disease and IBD is a dysfunctional immune system that attacks the gut. But there are likely multiple causes related to why this malfunction occurs in the first place. There have been several genetic variations associated with the development of Crohn’s disease, for example. But it is also suspected that certain infections can also trigger Crohn’s disease, while other microbes can aggravate the disease.

This new study, led by researchers at New York University, attempted to examine the interaction of these risk factors. They studied mice bred to have a mutation linked to Crohn’s disease, as well as cultured human intestinal cells from people with Crohn’s disease. The mice were exposed to norovirus, which is one of the most common causes of foodborne illness in humans. In these mice, the infection led to an increased risk of intestinal damage and the loss of certain cells in the small intestine, called Paneth cells, which help provide the first line of defense against infection. Jloss of inheritance or dysfunction appears play a driving role in the onset of Crohn’s disease along the small intestine.

The researchers also identified a protein produced by certain T cells known as inhibitor of apoptosis 5, or API5, which may provide protection against Crohn’s disease. In their mice, norovirus infection appears to damage Paneth cells by inhibiting API secretion5 from T lymphocytes.

To further test this hypothesis, the team introduced the protein into mice with Crohn’s disease, finding that all of the treated mice survived while only half of the untreated mice did. They also tested the protein on cells from the intestinal lining taken from Crohn’s disease patients with and without the mutation, finding that it only appeared to have a protective effect on cells from people with the mutation. . Finally, they found evidence that people with Crohn’s disease tend to have lower levels of T cells that produce API5.

The conclusions were published in Nature on Wednesday.

“What we found is really interesting,” study co-author Ken Cadwell, professor of microbiology at NYU Grossman School of Medicine, Told NBC News. “Unexpectedly, T cells protect the gut lining, and infectious triggers interfere with this ability.”

The results do not prove that norovirus is a smoking trigger for Crohn’s disease, so more research will be needed to validate what Cadwell and his team found here. IIt is likely that other common microbes can also trigger Crohn’s disease in susceptible people. A study last year, for example, suggested that a common yeast found in the gut may help cause or worsen IBD symptoms, but only when left unchecked. unchecked by the immune system. And there may be more genetic mutations that can increase the risk of these infections or other triggers for Crohn’s disease.

But if Cadwell’s research continues to show that API5 can short-circuit the complicated chain of events that leads to Crohn’s disease, it could indicate to more effective or easier to tolerate treatments one day. Standard drugs for Crohn’s disease generally work by weakening or suppressing the immune system, which can increase the risk of infections in general or other serious complications.

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