Fighting gut infections helps prevent Crohn’s disease and ulcerative colitis
A research team at the Montreal Heart Institute and Université de Montréal has shown that genes present in specific intestinal cells protect against the development of inflammatory bowel diseases. Published today in the scientific journal Genome Medicine, the study results show that more than a dozen of these genes, which contribute to the development of Crohn’s disease and ulcerative colitis, help fight viral and bacterial infections.
Crohn’s disease and ulcerative colitis, known as inflammatory bowel diseases, are characterized by chronic digestive system inflammation. The research team screened 145 genes associated with inflammatory bowel diseases (IBD) risk in human digestive system cells, called intestinal epithelial cells, and found that many of these genes are significant in helping these cells detect bacteria or viruses and set up the appropriate defensive response to control such infections. Thus, researchers have identified genes that make people more likely to develop chronic gut inflammation, characteristic of IBD when disrupted by genetic variants.
“Most of the current medical therapies used to treat Crohn’s disease and ulcerative colitis target the functions of immune system cells,” said Dr. John D. Rioux, an MHI researcher, medical professor at UdeM and Canada Research Chair in Genetics and Genomic Medicine. “This study demonstrates the importance of developing therapeutic approaches aimed at strengthening the protective functions of the digestive system for the benefit of patients with inflammatory bowel disease.”
10,000 new cases a year
More than 270,000 people suffer from IBD in Canada and almost 10,000 new cases appear every year, resulting in estimated annual economic costs of $2.6 billion. IBD is characterized by the body’s own immune system attacking parts of the digestive system. The exact causes of these diseases are still unknown, and there is currently no cure.
Previous genetic studies had already identified some differences in the genetic code associated with the development of IBD, but for most of them no actual disease-causing gene has been found.
“The challenge was how to use this genetic information to better understand the biological pathways leading to IBD,” said Jessy Carol Ntunzwenimana, a doctoral student at the Rioux Lab and co-lead author of the study. Her research team had therefore to develop a new approach to identify which genes are likely to be involved in IBD and reveal their biological functions.
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