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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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) |
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Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
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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 |
work_keys_str_mv |
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