Contributors: Biologie et Pathogénicité fongiques - Fungal Biology and Pathogenicity (BPF); Institut Pasteur Paris (IP)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE); University of Aberdeen; BIOASTER Microbiology Technology Institute Lyon; École Doctorale Bio Sorbonne Paris Cité Paris (ED562 - BioSPC); Université Sorbonne Paris Cité (USPC)-Université Paris Cité (UPCité); Leibniz Institute for Natural Product Research and Infection Biology (Hans Knoell Institute); Friedrich-Schiller-Universität = Friedrich Schiller University Jena Jena, Germany; ProDigest BVBA; Partenaires INRAE; Universiteit Gent = Ghent University (UGENT); Universität Zürich Zürich = University of Zurich (UZH); Mimetas; Radboud University Medical Center Nijmegen; Vall d'Hebron University Hospital Barcelona; Magic Bullet Consulting; Unité Mixte de Recherche sur le Fromage (UMRF); VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Clermont Auvergne (UCA); Nexbiome Therapeutics Clermont-Ferrand; University of Exeter; We received funding from the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie action, Innovative Training Network: FunHoMic; grant N° 812969. CdE received funding from the French Government ‘Investissement d'Avenir’ program (Laboratoire d'Excellence Integrative Biology of Emerging Infectious Diseases, ANR-10-LABX-62-IBEID), the Agence Nationale de la Recherche (ERA-Net Infect-ERA, FUNCOMPATH, ANR-14-IFEC-0004), the EU Horizon2020 consortium ‘Host-Directed Medicine in invasive FUNgal infections’—HDM-FUN (Grant Agreement 847507). SLL and CdE received funding from the Swiss National Science Foundation (Sinergia program, #CRSII5_173863). BIOASTER received funding from the French Government ‘Investissement d'Avenir’ program (Grant No. ANR-10-AIRT-03). MSG was supported by a Humboldt Research Fellowship for Postdoctoral Researchers by the Alexander von Humboldt-Foundation and the Deutsche Forschungsgemeinschaft (DFG) Emmy Noether Program (project no. 434385622/GR 5617/1-1). BH was supported by the Deutsche Forschungsgemeinschaft (DFG) project Hu 532/20-1, project C1 within the Collaborative Research Centre (CRC)/Transregio 124 FungiNet and the Balance of the Microverse Cluster under Germany´s Excellence Strategy—EXC 2051–Project-ID 390713860, the EU Horizon2020 consortium ‘Host-Directed Medicine in invasive FUNgal infections’—HDM-FUN (Grant Agreement 847507), the Leibniz Association Campus InfectoOptics SAS-2015-HKI-LWC and the Wellcome Trust (215599/Z/19/Z). IDJ was supported by the Deutsche Forschungsgemeinschaft (DFG) project C5 within the Collaborative Research Centre (CRC)/Transregio 124 FungiNet and the Balance of the Microverse Cluster under Germany´s Excellence Strategy—EXC 2051–Project-ID 390713860, the Leibniz Association Campus InfectoOptics SAS-2015-HKI-LWC and the Wellcome Trust (Grant 215599/Z/19/Z). CM received funding from the the Instituto de Salud Carlos III/FEDER. MGN was supported by an ERC Advanced Grant (#833247) and a Spinoza grant of the Netherlands Organization for Scientific Research. CAM was supported by EU Horizon2020 consortium ‘Host-Directed Medicine in invasive FUNgal infections’—HDM-FUN (Grant Agreement 847507) and the Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology (097377/Z/11/Z). AWW receives core funding support from the Scottish Government's Rural and Environment Science and Analytical Services (RESAS). AJPB was supported by a programme grant from the UK Medical Research Council (MR/M026663/1) and by the Medical Research Council Centre for Medical Mycology at the University of Exeter (MR/N006364/1).; ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010); ANR-14-IFEC-0004,FunComPath,From fungal commensalism to pathogenicity:dissection of the colonization-to-infection shift of Candida albicans(2014); ANR-10-AIRT-0003,BIOASTER,BIOASTER(2010); European Project: 812969,H2020-MSCA-ITN-2018,FunHoMic(2019); European Project: 847507,H2020-SC1-2019-Two-Stage-RTD,HDM-FUN(2020)
نبذة مختصرة : International audience ; 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.
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