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Article | Open Access

Candida albicans overgrowth disrupts the gut microbiota in mice bearing oral cancer

Xu Wanga,b, Shuangshaung Wua, Linman Lia, Zhimin Yana( )
Department of Oral Medicine, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China
Central Laboratory, Peking University School and Hospital of Stomatology, Beijing, China
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Abstract

Candida albicans is one of the most common opportunistic fungi in cancer patients. This study explored the influence of C. albicans on gut microbiota in oral tumour-bearing mice by means of 16S rRNA sequencing and ITS sequencing. It was found that C. albicans infection induced the decrease of alpha diversity of bacteria and fungi in the gut microbiome. For the bacteria, C. albicans caused the reduction of Ralstonia, Alistipes, Clostridia UCG-014, Ruminococcus, and Lachnospiraceae NK4A136 group. For the fungi, C. albicans inhibited the growth of other fungi including Aspergillus, Cladosporium, and Bipolaris. The neutralisation of γδT cells partly alleviated the out-of-balance of Firmicutes/Bacteroidota (F/B) ratio in the gut caused by C. albicans infection. However, γδT cell neutralisation boosted the overgrowth of C. albicans. Additionally, IL-17A neutralisation aggravated the microbial dysbiosis of bacteria and fungi caused by C. albicans infection. Further analysis indicated that C. albicans overgrowth might influence the correlations between fungal and bacterial kingdoms. In conclusion, C. albicans infection disturbed the gut microbiota of both bacteria and fungi in oral tumour-bearing mice, which may be associated with the intestinal immune components including γδT cells and IL-17A.

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Mycology
Pages 57-69

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Cite this article:
Wang X, Wu S, Li L, et al. Candida albicans overgrowth disrupts the gut microbiota in mice bearing oral cancer. Mycology, 2024, 15(1): 57-69. https://doi.org/10.1080/21501203.2023.2256761

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Received: 09 July 2023
Accepted: 04 September 2023
Published: 26 October 2023
© 2023 The Author(s).

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.