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

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...

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Published inMycology Vol. 15; no. 1; pp. 57 - 69
Main Authors Wang, Xu, Wu, Shuangshaung, Li, Linman, Yan, Zhimin
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 02.01.2024
Taylor & Francis Ltd
Taylor & Francis Group
Subjects
Aspergillus
Bacteria
Bipolaris
Cancer
Candida albicans
Cladosporium
Digestive system
Dysbacteriosis
dysbiosis
Fungi
Gastrointestinal tract
Gut microbiota
IL-17A
Infections
interleukin-17
Intestinal microflora
intestinal microorganisms
intestines
Lachnospiraceae
Microbiomes
Microbiota
Microorganisms
mouth neoplasms
mycology
neutralization
Oral cancer
Ralstonia
rRNA 16S
Ruminococcus
species diversity
Tumors
γδt cells
Candida albicans
IL-17A
γδt cells
gut microbiota
oral cancer
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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.
AbstractList is one of the most common opportunistic fungi in cancer patients. This study explored the influence of on gut microbiota in oral tumour-bearing mice by means of 16S rRNA sequencing and ITS sequencing. It was found that infection induced the decrease of alpha diversity of bacteria and fungi in the gut microbiome. For the bacteria, caused the reduction of , , , , and . For the fungi, inhibited the growth of other fungi including , , and . The neutralisation of γδT cells partly alleviated the out-of-balance of / (F/B) ratio in the gut caused by infection. However, γδT cell neutralisation boosted the overgrowth of . Additionally, IL-17A neutralisation aggravated the microbial dysbiosis of bacteria and fungi caused by infection. Further analysis indicated that overgrowth might influence the correlations between fungal and bacterial kingdoms. In conclusion, 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.
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.
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.
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.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.
Author Wang, Xu
Yan, Zhimin
Wu, Shuangshaung
Li, Linman
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  email: yzhimin96@163.com
  organization: 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
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Issue 1
Keywords Candida albicans
IL-17A
γδt cells
gut microbiota
oral cancer
Language English
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Snippet 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...
is one of the most common opportunistic fungi in cancer patients. This study explored the influence of on gut microbiota in oral tumour-bearing mice by means...
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...
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StartPage 57
SubjectTerms Aspergillus
Bacteria
Bipolaris
Cancer
Candida albicans
Cladosporium
Digestive system
Dysbacteriosis
dysbiosis
Fungi
Gastrointestinal tract
Gut microbiota
IL-17A
Infections
interleukin-17
Intestinal microflora
intestinal microorganisms
intestines
Lachnospiraceae
Microbiomes
Microbiota
Microorganisms
mouth neoplasms
mycology
neutralization
Oral cancer
Ralstonia
rRNA 16S
Ruminococcus
species diversity
Tumors
γδt cells
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Title Candida albicans overgrowth disrupts the gut microbiota in mice bearing oral cancer
URI https://www.tandfonline.com/doi/abs/10.1080/21501203.2023.2256761
https://www.ncbi.nlm.nih.gov/pubmed/38558840
https://www.proquest.com/docview/3092107819
https://www.proquest.com/docview/3031133113
https://www.proquest.com/docview/3040454889
https://pubmed.ncbi.nlm.nih.gov/PMC10977010
https://doaj.org/article/831d4574474746439d818443b9551576
Volume 15
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