This conclusion was reached by researchers from the Weill Cornell Medical College (USA), whose article published in the journal Nature.
Experts do not yet know exactly the biological causes underlying the development of inflammatory bowel disease (IBD) – a chronic inflammatory process that affects the mucous membrane of the gastrointestinal tract. Two main types of IBD – Crohn’s disease and ulcerative colitis. It is believed that these diseases are of an autoimmune nature – abnormal activity of the immune system leads to the production of antibodies to the cells of the intestinal mucosa. Therefore, patients are prescribed steroid hormones that suppress the activity of the immune system, however, for reasons still unclear, this method of therapy does not always work.
Immunologist Iliyan Iliev and his colleagues have previously found that the development of IBD may be associated with a certain composition of the mycobiota – a community of fungi that live in the body in general and in the gastrointestinal tract in particular. However, exactly how the mycobiota causes inflammation in the gut was unclear.
In a new study, scientists studied strains (genetic variants) of the yeast-like fungus Candida albicans that inhabit the intestines of healthy people and patients with ulcerative colitis. Candida albicans is a natural part of the human microflora.
It turned out that the strains of this fungus differ from each other in the same way as the people in whose intestines they live differ from each other. At the same time, in patients with ulcerative colitis, the intestines are not only more affected by the fungus than in healthy people, the strains of Candida albicans present in their intestines are particularly harmful, as they produce the candidalin toxin, which in a certain way affects immune cells, provoking inflammation. Moreover, the more severe the course of the disease, the stronger the inflammation, the more likely the presence of toxic variants of the fungus in the intestine.
Researchers have found that in the presence of pathogenic strains of Candida albicans, anti-inflammatory drugs cease to work, which may explain why steroids do not help all patients with IBD. In general, Iliev and his colleagues concluded that in a person with a normally functioning immune system, toxic variants of the fungus by themselves are not capable of causing intestinal inflammation. However, if inflammation has already begun, pathogenic strains of Candida albicans begin to actively multiply in the gastrointestinal tract and provoke the development of the disease, interfering with its treatment.
This discovery raises hopes for the development of personalized therapies for IBD that target toxic strains of fungi living in the intestines of patients, Iliev and his colleagues hope.
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