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Fungal aggravation
The gut microbiota includes 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 alterations in the gut microbiota in mice with mucosal lesions and human subjects with Crohn’s disease, Jain et al. discovered the mushroom Debaryomyces hansenii localized to wounds in inflamed mucous tissues (see the perspective of Chiaro and Round). Impaired wound healing was associated with antibiotic treatment, proliferation of the fungus, and subsequent induction of a type I interferon-CCL5 axis by macrophages. The fungus has been observed in macrophages. Such a persistent injury stimulus is a hallmark of inflammatory bowel disease, including Crohn’s disease and ulcerative colitis. It is not known whether this salt tolerant fungus is a natural symbiont, but it is used in the food industry for the surface refining of cheese and meat products.
Science, this issue p. 1154; see also p. 1102
Abstract
The alterations in the composition of the mycobiota associated with Crohn’s disease (CD) are difficult to associate with determinants of pathophysiology, such as poor wound repair. Using culture dependent and independent methods, we found that Debaryomyces hansenii preferentially localized and abundant in incompletely healed intestinal wounds of mice and inflamed mucous tissues of human subjects with CD. D. hansenii cultures of injured mice and inflamed CD tissue impaired colon healing when introduced into injured mice reared conventionally or gnotobiotic. We re-isolated D. hansenii injured areas of these mice, responding to Koch’s postulates. Mechanically, D. hansenii alteration of mucosal healing by the type 1 interferon axis specific to myeloid cells and CCL5. Taken together, we have identified a fungus that inhabits inflamed CD tissue and can lead to deregulated mucosal scarring.
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