Epithelial hypoxia maintains colonization resistance against Candida albicans.

Autor:	Savage HP; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Bays DJ; Department of Internal Medicine, Division of Infectious Diseases, School of Medicine, University of California, Davis, Sacramento, CA 95817, USA., Tiffany CR; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Gonzalez MAF; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Bejarano EJ; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Carvalho TP; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA; Departamento de Clinica e Cirurgia Veterinárias, Escola de Veterinária da Universidade Federal de Minas Gerais, Universidade Federal de Minas Gerais, Av. Antonio Carlos, 6627 Belo Horizonte, MG, Brazil., Luo Z; Department of Pathology Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA., Masson HLP; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Nguyen H; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA., Santos RL; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA; Departamento de Clinica e Cirurgia Veterinárias, Escola de Veterinária da Universidade Federal de Minas Gerais, Universidade Federal de Minas Gerais, Av. Antonio Carlos, 6627 Belo Horizonte, MG, Brazil., Reagan KL; Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95615, USA., Thompson GR; Department of Internal Medicine, Division of Infectious Diseases, School of Medicine, University of California, Davis, Sacramento, CA 95817, USA., Bäumler AJ; Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA. Electronic address: ajbaumler@ucdavis.edu.
Jazyk:	angličtina
Zdroj:	Cell host & microbe [Cell Host Microbe] 2024 Jul 10; Vol. 32 (7), pp. 1103-1113.e6. Date of Electronic Publication: 2024 Jun 04.
DOI:	10.1016/j.chom.2024.05.008
Abstrakt:	Antibiotic treatment promotes the outgrowth of intestinal Candida albicans, but the mechanisms driving this fungal bloom remain incompletely understood. We identify oxygen as a resource required for post-antibiotic C. albicans expansion. C. albicans depleted simple sugars in the ceca of gnotobiotic mice but required oxygen to grow on these resources in vitro, pointing to anaerobiosis as a potential factor limiting growth in the gut. Clostridia species limit oxygen availability in the large intestine by producing butyrate, which activates peroxisome proliferator-activated receptor gamma (PPAR-γ) signaling to maintain epithelial hypoxia. Streptomycin treatment depleted Clostridia-derived butyrate to increase epithelial oxygenation, but the PPAR-γ agonist 5-aminosalicylic acid (5-ASA) functionally replaced Clostridia species to restore epithelial hypoxia and colonization resistance against C. albicans. Additionally, probiotic Escherichia coli required oxygen respiration to prevent a post-antibiotic bloom of C. albicans, further supporting the role of oxygen in colonization resistance. We conclude that limited access to oxygen maintains colonization resistance against C. albicans. Competing Interests: Declaration of interests G.R.T. is consulting for Astellas, Cidara, F2G, Immy, Mayne, Melinta, Mundipharma, Scynexis, and Pfizer on projects that are not related to this publication. G.R.T. receives research support from Astellas, Cidara, F2G, Mayne, Melinta, Merck, Mundipharma, Scynexis, and Pfizer for projects that are not related to this publication. (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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