Fungal aggravation
The intestinal microbiota contains not only prokaryotes, viruses, protists and sometimes helminths, but also fungi. The role that fungi play in this symbiosis has long been overlooked. While investigating changes to the intestinal microbiota in mice with mucosal damage and in people with Crohn’s disease, Jain said. et al. discover the fungus Debaryomyces hansenii localized to wounds in inflamed mucosal tissue (see the perspective of Chiaro and Round). Impaired healing was associated with antibiotic treatment, fungal overgrowth and subsequent induction of a type I interferon – CCL5 axis by macrophages. The fungus was observed within macrophages. Such persistent injury stimulus is a hallmark of inflammatory bowel disease, including Crohn’s disease and ulcerative colitis. It is not known if this salt tolerant fungus is a natural symbion, but it is used in the food industry for the ripening of cheese and meat products.
Science, this issue p. 1154; see also p. 1102
Abstract
Changes in the mycobiota composition associated with Crohn’s disease (CD) are difficult to associate with defining elements of pathophysiology, such as poor recovery from injuries. Using culture-dependent and -independent methods, we discovered this Debaryomyces hansenii preferably localized in and was abundant in incompletely intestinal intestinal wounds of mice and inflamed mucosal tissues of CD human subjects. D. hansenii cultures of injured mice and inflamed CD tissues affected the healing of the colon when it was introduced into injured conventional or gnotobiotic mice. We insulated again D. hansenii from injured areas of these mice, fulfilling Koch’s postulations. Mechanical, D. hansenii impaired healing of the mucosa by the myeloid cell-specific type 1 interferon – CCL5 axis. Together, we identified a fungus that lives in inflamed CD tissue and can lead to unregulated mucosal healing.