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A nasty but short-lived gastrointestinal bug can have lasting consequences for some unlucky ones. Researchers have found evidence in mice and human cells that norovirus infection can trigger Crohn’s disease in people who are already genetically predisposed to it. The results 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 commonly in the small intestine. Symptoms can vary greatly in severity, but commonly include diarrhea, weight loss, and severe stomach cramps. Sufferers also tend to experience flare-ups, with symptoms returning or worsening. About 3 million Americans are Thought having IBD.
The underlying mechanism behind Crohn’s disease and IBD is a dysfunctional immune system attacking the gut. But there are likely several, interconnected causes as to why this dysfunction occurs in the first place. For example, there have been several genetic variations that have been linked to the development of Crohn’s disease. But it is also suspected that some infections can also trigger Crohn’s disease other microbes can make the disease worse.
This new study, led by researchers from New York University, attempted to examine the interaction of these risk factors. They looked at mice that were bred to have a mutation linked to Crohn’s disease and 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 a greater risk of intestinal damage and the loss of certain cells in the small intestine, called Paneth cells, the help provide the first line of defense against infection. TLoss of heir or dysfunction appears to play a driving role in the development of Crohn’s disease along the small intestine.
The researchers also identified a Protein produced by certain T cells known as apoptosis inhibitor 5 or API5, which may provide protection against Crohn’s disease. In their mice, norovirus infection appeared to damage Paneth cells by inhibiting the secretion of API5 of T cells.
To further test this hypothesis, the team introduced the protein to mice with Crohn’s disease and found that all treated mice survived, while only half of the untreated mice survived. They also tested the protein on gut lining cells from Crohn’s patients with and without the mutation and found that it only appeared to have a protective effect on the cells of people with the mutation. Eventually, they found evidence that people with Crohn’s disease tend to have fewer T cells that produce API5.
The insights were released in nature Wednesday.
“What we found is really interesting,” said study co-author Ken Cadwell, professor of microbiology at NYU Grossman School of Medicine. said NBC News. “In an unexpected way, T cells protect the gut lining, and infectious triggers impair this ability.”
The results don’t prove that norovirus is a trigger for Crohn’s disease, so more research is needed to validate what Cadwell and his team found here. IIt is likely that other common microbes can also trigger Crohn’s disease in at-risk individuals. For example, a study last year suggested that common yeast in the gut may help cause or worsen IBD symptoms, but only if left over unchecked through the immune system. And there may be other genetic mutations that can increase your risk of these infections or other factors that trigger Crohn’s disease.
But if Cadwell’s research continues to show that API5 can short-circuit the complicated chain of events that lead to Crohn’s disease, it could be a clue to more effective or more tolerable treatments one day. standard drugs for Crohn’s usually work by weakening or suppressing the immune system, which can increase the general risk of infection or other serious complications.
