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Fragile balance in the gut

Candida albicans hyphae on intestinal epithelial cells
Candida albicans(yellow) forming hyphae on differentiated intestinal epithelial cells (nuclei in blue and F-actin in purple. Source: Raquel Alonso-Roman / Leibniz-HKI

The yeast Candida albicans naturally colonizes the human body, especially common in the intestine. Usually this is a benign colonization, as the immune system and a healthy gut microbiome keep it in check. However, if the microbiome gets out of balance or the immune system is severely compromised, C. albicans can enter the bloodstream. This can be life-threatening especially for immunocompromised people in intensive care units.

Researchers at Leibniz-HKI have now found that human intestinal cells play an important role in fighting fungal infections caused by C. albicans. "The intestinal cells nourish lactic acid bacteria, which thereby multiply and in turn take nutrients away from the yeast fungus," explains first author Raquel Alonso-Roman, member of the Cluster of Excellence Balance of the Microverse. The new conditions force C. albicans to adapt its metabolism, causing it to shed certain characteristics and  making it less infectious. Adding the probiotics to the gut creates a balance between yeast, lactic acid bacteria and the rest of the microbiome, which restores a healthy state.

Infections with C. albicans, such as vulvovaginal infections, are already successfully treated with lactic acid bacteria. "We already know that lactic acid bacteria in particular can counteract a fungal infection, prevent it or even kill the fungus. Our work now addresses the question of 'how'," explains Bernhard Hube, head of the Department of Microbial Pathogenicity Mechanisms.


Read more in the latest press release by Nora Brakhage (Leibniz-HKI)



Alonso-Roman R, Last A, Mirhakkak M.H, Sprague J.L, Möller L, Großmann P, Graf K, Gratz R, Mogavero S, Vylkova S, Panagiotou G, Schäuble S, Hube B, Gresnigt M.S (2022) Lactobacillus rhamnosus colonisation antagonizes Candida albicans by forcing metabolic adaptations that compromise pathogenicity. Nature Communications, doi: 10.1038/s41467-022-30661-5