PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.

PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.

We recently showed that IL-13 or peroxisome proliferator activated receptor gamma (PPARgamma) ligands attenuate Candida albicans colonization of the gastrointestinal tract. Here, using a macrophage-specific Dectin-1 deficient mice model, we demonstrate that Dectin-1 is essential to control fungal ga...

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Autores principales: Amandine Galès, Annabelle Conduché, José Bernad, Lise Lefevre, David Olagnier, Maryse Béraud, Guillaume Martin-Blondel, Marie-Denise Linas, Johan Auwerx, Agnès Coste, Bernard Pipy
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2010
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Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Acceso en línea:https://doaj.org/article/6493e3dd10ed4b16ac832988879bbc14
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spelling oai:doaj.org-article:6493e3dd10ed4b16ac832988879bbc142021-11-25T05:48:24ZPPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.1553-73661553-737410.1371/journal.ppat.1000714https://doaj.org/article/6493e3dd10ed4b16ac832988879bbc142010-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20062524/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374We recently showed that IL-13 or peroxisome proliferator activated receptor gamma (PPARgamma) ligands attenuate Candida albicans colonization of the gastrointestinal tract. Here, using a macrophage-specific Dectin-1 deficient mice model, we demonstrate that Dectin-1 is essential to control fungal gastrointestinal infection by PPARgamma ligands. We also show that the phagocytosis of yeast and the release of reactive oxygen intermediates in response to Candida albicans challenge are impaired in macrophages from Dectin-1 deficient mice treated with PPARgamma ligands or IL-13. Although the Mannose Receptor is not sufficient to trigger antifungal functions during the alternative activation of macrophages, our data establish the involvement of the Mannose Receptor in the initial recognition of non-opsonized Candida albicans by macrophages. We also demonstrate for the first time that the modulation of Dectin-1 expression by IL-13 involves the PPARgamma signaling pathway. These findings are consistent with a crucial role for PPARgamma in the alternative activation of macrophages by Th2 cytokines. Altogether these data suggest that PPARgamma ligands may be of therapeutic value in esophageal and gastrointestinal candidiasis in patients severely immunocompromised or with metabolic diseases in whom the prevalence of candidiasis is considerable.Amandine GalèsAnnabelle ConduchéJosé BernadLise LefevreDavid OlagnierMaryse BéraudGuillaume Martin-BlondelMarie-Denise LinasJohan AuwerxAgnès CosteBernard PipyPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 6, Iss 1, p e1000714 (2010)
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
Amandine Galès
Annabelle Conduché
José Bernad
Lise Lefevre
David Olagnier
Maryse Béraud
Guillaume Martin-Blondel
Marie-Denise Linas
Johan Auwerx
Agnès Coste
Bernard Pipy
PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
description We recently showed that IL-13 or peroxisome proliferator activated receptor gamma (PPARgamma) ligands attenuate Candida albicans colonization of the gastrointestinal tract. Here, using a macrophage-specific Dectin-1 deficient mice model, we demonstrate that Dectin-1 is essential to control fungal gastrointestinal infection by PPARgamma ligands. We also show that the phagocytosis of yeast and the release of reactive oxygen intermediates in response to Candida albicans challenge are impaired in macrophages from Dectin-1 deficient mice treated with PPARgamma ligands or IL-13. Although the Mannose Receptor is not sufficient to trigger antifungal functions during the alternative activation of macrophages, our data establish the involvement of the Mannose Receptor in the initial recognition of non-opsonized Candida albicans by macrophages. We also demonstrate for the first time that the modulation of Dectin-1 expression by IL-13 involves the PPARgamma signaling pathway. These findings are consistent with a crucial role for PPARgamma in the alternative activation of macrophages by Th2 cytokines. Altogether these data suggest that PPARgamma ligands may be of therapeutic value in esophageal and gastrointestinal candidiasis in patients severely immunocompromised or with metabolic diseases in whom the prevalence of candidiasis is considerable.
format article
author Amandine Galès
Annabelle Conduché
José Bernad
Lise Lefevre
David Olagnier
Maryse Béraud
Guillaume Martin-Blondel
Marie-Denise Linas
Johan Auwerx
Agnès Coste
Bernard Pipy
author_facet Amandine Galès
Annabelle Conduché
José Bernad
Lise Lefevre
David Olagnier
Maryse Béraud
Guillaume Martin-Blondel
Marie-Denise Linas
Johan Auwerx
Agnès Coste
Bernard Pipy
author_sort Amandine Galès
title PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
title_short PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
title_full PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
title_fullStr PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
title_full_unstemmed PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.
title_sort pparγ controls dectin-1 expression required for host antifungal defense against candida albicans.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/6493e3dd10ed4b16ac832988879bbc14
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