In an article published in Clin Gastroenterol, researchers suggested intestinal fungi (molds and yeasts) growth may play an important role in aggravating Crohn’s disease (CD). The scientists studied organisms in the intestines and feces was conducted in 19 Crohn’s disease patients and 7 healthy controls. They found many fungal inhabitants, such as C. albicans, A. clavatus, and C. neoformans; however, their functional roles are as yet unknown in CD.
Compared to the healthy controls, the Crohn’s disease patients had significantly higher levels of several mycotoxin-producing fungi including Candida species, Cryptococcus neoformans, Aspergillus clavatus, and Gibberalla monilformis. In addition, significantly higher levels of both fungi and inflammatory cytokines (such as tumor necrosis factor α, interferon-γ, and interleukin-10) were seen in the inflamed versus non-inflamed intestinal tissue of the Crohn’s patients.
Intestinal balance is sustained by a constant crosstalk between the intestinal microbiota and the host. An alteration in gut bacterial microbiota composition can disrupt the mutual relationship of these 2 partners, leading to chronic bowel disorders. Perturbation of intestinal homeostasis is thus believed to play a pivotal role in the pathogenesis of CD.6–8
It is not surprising that gut fungal community, as an important component of bowel flora, also contributes to microbial immune homeostasis. For instance, C. albicans can promote immune tolerance, whereas overgrowth of this fungus results in mucosal candidiasis and gut inflammation.
Therefore, the fungal microbiota might be actively involved in the balance between inflammation and tolerance at mucosal surfaces in CD. The changes in the host-fungus interplay might be one of the mechanisms underlying CD. In addition, our results highlight the presence of unprecedented intestinal fungal inhabitants, such as C. albicans, A. clavatus, and C. neoformans; however, their functional roles are as yet unknown in CD.
It would be an important implication to distinguish which fungal species may be a cause required for CD, or a sign resulting from this disease.
The researchers concluded, “This study first demonstrates that the fungal microbiota in the inflamed mucosa is distinguishable from that of the noninflamed area. Shifts of gut fungal microbiota composition may be associated with mucosal inflammation and disease activity of CD. Our data would provide novel insights into understanding the potential of gut fungal microbiota in the pathogenesis of CD.
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