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Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing

Candida albicans is a commensal yeast of the human gut which is tolerated by the immune system but has the potential to become an opportunistic pathogen. One way in which C. albicans achieves this duality is through concealing or exposing cell wall pathogen-associated molecular patterns (PAMPs) in r...

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Autores principales: Cottier, Fabien, Sherrington, Sarah, Cockerill, Sarah, del Olmo Toledo, Valentina, Kissane, Stephen, Tournu, Helene, Orsini, Luisa, Palmer, Glen E., Pérez, J. Christian, Hall, Rebecca A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Microbiology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6794483/
https://www.ncbi.nlm.nih.gov/pubmed/31615961
http://dx.doi.org/10.1128/mBio.02347-19
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author Cottier, Fabien
Sherrington, Sarah
Cockerill, Sarah
del Olmo Toledo, Valentina
Kissane, Stephen
Tournu, Helene
Orsini, Luisa
Palmer, Glen E.
Pérez, J. Christian
Hall, Rebecca A.
author_facet Cottier, Fabien
Sherrington, Sarah
Cockerill, Sarah
del Olmo Toledo, Valentina
Kissane, Stephen
Tournu, Helene
Orsini, Luisa
Palmer, Glen E.
Pérez, J. Christian
Hall, Rebecca A.
author_sort Cottier, Fabien
collection PubMed
description Candida albicans is a commensal yeast of the human gut which is tolerated by the immune system but has the potential to become an opportunistic pathogen. One way in which C. albicans achieves this duality is through concealing or exposing cell wall pathogen-associated molecular patterns (PAMPs) in response to host-derived environment cues (pH, hypoxia, and lactate). This cell wall remodeling allows C. albicans to evade or hyperactivate the host’s innate immune responses, leading to disease. Previously, we showed that adaptation of C. albicans to acidic environments, conditions encountered during colonization of the female reproductive tract, induces significant cell wall remodeling resulting in the exposure of two key fungal PAMPs (β-glucan and chitin). Here, we report that this pH-dependent cell wall remodeling is time dependent, with the initial change in pH driving cell wall unmasking, which is then remasked at later time points. Remasking of β-glucan was mediated via the cell density-dependent fungal quorum sensing molecule farnesol, while chitin remasking was mediated via a small, heat-stable, nonproteinaceous secreted molecule(s). Transcript profiling identified a core set of 42 genes significantly regulated by pH over time and identified the transcription factor Efg1 as a regulator of chitin exposure through regulation of CHT2. This dynamic cell wall remodeling influenced innate immune recognition of C. albicans, suggesting that during infection, C. albicans can manipulate the host innate immune responses.
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spelling pubmed-67944832019-10-21 Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing Cottier, Fabien Sherrington, Sarah Cockerill, Sarah del Olmo Toledo, Valentina Kissane, Stephen Tournu, Helene Orsini, Luisa Palmer, Glen E. Pérez, J. Christian Hall, Rebecca A. mBio Research Article Candida albicans is a commensal yeast of the human gut which is tolerated by the immune system but has the potential to become an opportunistic pathogen. One way in which C. albicans achieves this duality is through concealing or exposing cell wall pathogen-associated molecular patterns (PAMPs) in response to host-derived environment cues (pH, hypoxia, and lactate). This cell wall remodeling allows C. albicans to evade or hyperactivate the host’s innate immune responses, leading to disease. Previously, we showed that adaptation of C. albicans to acidic environments, conditions encountered during colonization of the female reproductive tract, induces significant cell wall remodeling resulting in the exposure of two key fungal PAMPs (β-glucan and chitin). Here, we report that this pH-dependent cell wall remodeling is time dependent, with the initial change in pH driving cell wall unmasking, which is then remasked at later time points. Remasking of β-glucan was mediated via the cell density-dependent fungal quorum sensing molecule farnesol, while chitin remasking was mediated via a small, heat-stable, nonproteinaceous secreted molecule(s). Transcript profiling identified a core set of 42 genes significantly regulated by pH over time and identified the transcription factor Efg1 as a regulator of chitin exposure through regulation of CHT2. This dynamic cell wall remodeling influenced innate immune recognition of C. albicans, suggesting that during infection, C. albicans can manipulate the host innate immune responses. American Society for Microbiology 2019-10-15 /pmc/articles/PMC6794483/ /pubmed/31615961 http://dx.doi.org/10.1128/mBio.02347-19 Text en Copyright © 2019 Cottier et al. https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Article
Cottier, Fabien
Sherrington, Sarah
Cockerill, Sarah
del Olmo Toledo, Valentina
Kissane, Stephen
Tournu, Helene
Orsini, Luisa
Palmer, Glen E.
Pérez, J. Christian
Hall, Rebecca A.
Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title_full Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title_fullStr Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title_full_unstemmed Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title_short Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing
title_sort remasking of candida albicans β-glucan in response to environmental ph is regulated by quorum sensing
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6794483/
https://www.ncbi.nlm.nih.gov/pubmed/31615961
http://dx.doi.org/10.1128/mBio.02347-19
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