Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.

The β-glucan receptor Dectin-1 is a member of the C-type lectin family and functions as an innate pattern recognition receptor in antifungal immunity. In both mouse and man, Dectin-1 has been found to play an essential role in controlling infections with Candida albicans, a normally commensal fungus...

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Autores principales: Mohlopheni J Marakalala, Simon Vautier, Joanna Potrykus, Louise A Walker, Kelly M Shepardson, Alex Hopke, Hector M Mora-Montes, Ann Kerrigan, Mihai G Netea, Graeme I Murray, Donna M Maccallum, Robert Wheeler, Carol A Munro, Neil A R Gow, Robert A Cramer, Alistair J P Brown, Gordon D Brown
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/75074377bc0b44e9bd45a605a50f9aad
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spelling oai:doaj.org-article:75074377bc0b44e9bd45a605a50f9aad2021-11-18T06:05:45ZDifferential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.1553-73661553-737410.1371/journal.ppat.1003315https://doaj.org/article/75074377bc0b44e9bd45a605a50f9aad2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23637604/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The β-glucan receptor Dectin-1 is a member of the C-type lectin family and functions as an innate pattern recognition receptor in antifungal immunity. In both mouse and man, Dectin-1 has been found to play an essential role in controlling infections with Candida albicans, a normally commensal fungus in man which can cause superficial mucocutaneous infections as well as life-threatening invasive diseases. Here, using in vivo models of infection, we show that the requirement for Dectin-1 in the control of systemic Candida albicans infections is fungal strain-specific; a phenotype that only becomes apparent during infection and cannot be recapitulated in vitro. Transcript analysis revealed that this differential requirement for Dectin-1 is due to variable adaptation of C. albicans strains in vivo, and that this results in substantial differences in the composition and nature of their cell walls. In particular, we established that differences in the levels of cell-wall chitin influence the role of Dectin-1, and that these effects can be modulated by antifungal drug treatment. Our results therefore provide substantial new insights into the interaction between C. albicans and the immune system and have significant implications for our understanding of susceptibility and treatment of human infections with this pathogen.Mohlopheni J MarakalalaSimon VautierJoanna PotrykusLouise A WalkerKelly M ShepardsonAlex HopkeHector M Mora-MontesAnn KerriganMihai G NeteaGraeme I MurrayDonna M MaccallumRobert WheelerCarol A MunroNeil A R GowRobert A CramerAlistair J P BrownGordon D BrownPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 4, p e1003315 (2013)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Mohlopheni J Marakalala
Simon Vautier
Joanna Potrykus
Louise A Walker
Kelly M Shepardson
Alex Hopke
Hector M Mora-Montes
Ann Kerrigan
Mihai G Netea
Graeme I Murray
Donna M Maccallum
Robert Wheeler
Carol A Munro
Neil A R Gow
Robert A Cramer
Alistair J P Brown
Gordon D Brown
Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
description The β-glucan receptor Dectin-1 is a member of the C-type lectin family and functions as an innate pattern recognition receptor in antifungal immunity. In both mouse and man, Dectin-1 has been found to play an essential role in controlling infections with Candida albicans, a normally commensal fungus in man which can cause superficial mucocutaneous infections as well as life-threatening invasive diseases. Here, using in vivo models of infection, we show that the requirement for Dectin-1 in the control of systemic Candida albicans infections is fungal strain-specific; a phenotype that only becomes apparent during infection and cannot be recapitulated in vitro. Transcript analysis revealed that this differential requirement for Dectin-1 is due to variable adaptation of C. albicans strains in vivo, and that this results in substantial differences in the composition and nature of their cell walls. In particular, we established that differences in the levels of cell-wall chitin influence the role of Dectin-1, and that these effects can be modulated by antifungal drug treatment. Our results therefore provide substantial new insights into the interaction between C. albicans and the immune system and have significant implications for our understanding of susceptibility and treatment of human infections with this pathogen.
format article
author Mohlopheni J Marakalala
Simon Vautier
Joanna Potrykus
Louise A Walker
Kelly M Shepardson
Alex Hopke
Hector M Mora-Montes
Ann Kerrigan
Mihai G Netea
Graeme I Murray
Donna M Maccallum
Robert Wheeler
Carol A Munro
Neil A R Gow
Robert A Cramer
Alistair J P Brown
Gordon D Brown
author_facet Mohlopheni J Marakalala
Simon Vautier
Joanna Potrykus
Louise A Walker
Kelly M Shepardson
Alex Hopke
Hector M Mora-Montes
Ann Kerrigan
Mihai G Netea
Graeme I Murray
Donna M Maccallum
Robert Wheeler
Carol A Munro
Neil A R Gow
Robert A Cramer
Alistair J P Brown
Gordon D Brown
author_sort Mohlopheni J Marakalala
title Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
title_short Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
title_full Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
title_fullStr Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
title_full_unstemmed Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1.
title_sort differential adaptation of candida albicans in vivo modulates immune recognition by dectin-1.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/75074377bc0b44e9bd45a605a50f9aad
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