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Lactobacillus rhamnosus colonisation antagonizes Candida albicans by forcing metabolic adaptations that compromise pathogenicity.

Abstract (Expand)

Intestinal microbiota dysbiosis can initiate overgrowth of commensal Candida species - a major predisposing factor for disseminated candidiasis. Commensal bacteria such as Lactobacillus rhamnosus can … antagonize Candida albicans pathogenicity. Here, we investigate the interplay between C. albicans, L. rhamnosus, and intestinal epithelial cells by integrating transcriptional and metabolic profiling, and reverse genetics. Untargeted metabolomics and in silico modelling indicate that intestinal epithelial cells foster bacterial growth metabolically, leading to bacterial production of antivirulence compounds. In addition, bacterial growth modifies the metabolic environment, including removal of C. albicans' favoured nutrient sources. This is accompanied by transcriptional and metabolic changes in C. albicans, including altered expression of virulence-related genes. Our results indicate that intestinal colonization with bacteria can antagonize C. albicans by reshaping the metabolic environment, forcing metabolic adaptations that reduce fungal pathogenicity.

Authors: R. Alonso-Roman, A. Last, M. H. Mirhakkak, J. L. Sprague, L. Moller, P. Grossmann, K. Graf, R. Gratz, S. Mogavero, S. Vylkova, G. Panagiotou, S. Schauble, B. Hube, M. S. Gresnigt

Date Published: 9th Jun 2022

Publication Type: Journal

The impact of the Fungus-Host-Microbiota interplay upon Candida albicans infections: current knowledge and new perspectives.

Abstract (Expand)

Candida albicans is a major fungal pathogen of humans. It exists as a commensal in the oral cavity, gut or genital tract of most individuals, constrained by the local microbiota, epithelial barriers … and immune defences. Their perturbation can lead to fungal outgrowth and the development of mucosal infections such as oropharyngeal or vulvovaginal candidiasis, and patients with compromised immunity are susceptible to life-threatening systemic infections. The importance of the interplay between fungus, host and microbiota in driving the transition from C. albicans commensalism to pathogenicity is widely appreciated. However, the complexity of these interactions, and the significant impact of fungal, host and microbiota variability upon disease severity and outcome, are less well understood. Therefore, we summarise the features of the fungus that promote infection, and how genetic variation between clinical isolates influences pathogenicity. We discuss antifungal immunity, how this differs between mucosae, and how individual variation influences a person's susceptibility to infection. Also, we describe factors that influence the composition of gut, oral and vaginal microbiotas, and how these affect fungal colonisation and antifungal immunity. We argue that a detailed understanding of these variables, which underlie fungal-host-microbiota interactions, will present opportunities for directed antifungal therapies that benefit vulnerable patients.

Authors: C. d'Enfert, A. K. Kaune, L. R. Alaban, S. Chakraborty, N. Cole, M. Delavy, D. Kosmala, B. Marsaux, R. Frois-Martins, M. Morelli, D. Rosati, M. Valentine, Z. Xie, Y. Emritloll, P. A. Warn, F. Bequet, M. E. Bougnoux, S. Bornes, M. S. Gresnigt, B. Hube, I. D. Jacobsen, M. Legrand, S. Leibundgut-Landmann, C. Manichanh, C. A. Munro, M. G. Netea, K. Queiroz, K. Roget, V. Thomas, C. Thoral, P. Van den Abbeele, A. W. Walker, A. J. P. Brown

Date Published: 24th Nov 2020

Publication Type: Not specified

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