A yeast commonly used by the food industry can colonize intestinal wounds in antibiotic-treated mice, promoting chronic inflammation and impaired wound healing - hallmark symptoms of inflammatory bowel diseases (IBD), a new study finds. What's more, the results show that the fungus, Debaryomyces hansenii, is also present in the inflamed intestinal tissues of human patients with Crohn's disease (CD). While it's unknown if D. hansenii is a natural resident of the commensal community or an invasive outsider, the results identify a fungus that provides a promising target for treating IBDs. Even as fungi make up a proportion of the gut microbiota, their role in microbiota-mediated processes, such as the impaired mucosal healing common to IBDs, has been long overlooked. While investigating alterations to the gut microbiota in mice with intestinal wounds and human subjects with CD, Umang Jain and colleagues found that D. hansenii preferentially colonized and thrived within inflamed intestinal tissues. According to Jain et al., fungus colonization was associated with antibiotic treatment, and once established, D. hansenii impaired wound healing in mice by promoting activation of the type I interferon-CCL5 pathway in surrounding macrophages. In sequencing studies of samples from six CD patients, the authors found a greater amount of the fungus in inflamed regions compared with uninflamed regions from the same patient. "The study of Jain et al. demonstrates that the loss of commensal microbes can open up niches for potentially harmful opportunistic organisms," write Daniel Altmann and colleagues in a related Perspective, findings which suggest that the use of antibiotics in individuals with chronic intestinal disease should be evaluated more carefully. "Because commensal microbes can influence multiple host pathways that include preventing inflammation, colonization of pathogens and promoting wound healing, specific cocktails of commensal bacteria might prove to be better therapeutic agents that act on several levels to protect from disease," Altmann et al. write.
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Science