Common Fungus may affect Crohn’s disease

By Emily Taketa

Malassezia yeasts are typically found near human hair follicles, but were recently found in a higher abundance in the gut of Crohn’s patients. David Underhill, the Janis and William Wetsman Family Chair in Inflammatory Bowel Disease at Cedars-Sinai in Los Angeles, and Jose Limon, a Cedars-Sinai research team member, investigated the connection between the fungi’s abundance in the gut and how it may potentially impact intestinal diseases. Their recent study, published in the Cell Host & Microbe Journal, found that the Malassezia restrica had a higher abundance in gut tissue samples in patients with intestinal diseases than healthy individuals. The availability of Malassezia is also known to indicate a gene variation that decreases an individual’s immunity to fungi. This same gene variation is more common in Crohn’s patients than healthy individuals which suggests a possible connection to intestinal health.            

The researchers initially found that the presence of these fungi worsened the intestinal inflammation in mice and the gene variation for immunity against this fungi was a useful treatment. In Crohn’s patients, the gene variation, called IBD CARD9 risk allele, increases the inflammatory cytokine production in human immune cells when exposed to Malassezia restrica and therefore more Malassezia were found in these patients’ intestinal tissues. When a patient already has intestinal inflammation Malassezia appears to increase the severity of the inflammation, as specifically seen in Crohn’s patients. However, the researchers are unclear whether Malassezia presence by itself, without prior inflammation, has a negative impact. These researchers hope to decrease the concentration of these Malassezia yeasts in Crohn’s patients to alleviate the negative intestinal symptoms in the future.

 

Cell Press. (2019, March 5). A fungus usually found on skin might play a role in Crohn's disease. ScienceDaily. Retrieved March 16, 2019 from www.sciencedaily.com/releases/2019/03/190305112836.htm