Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.

Chitin is an essential structural polysaccharide of fungal pathogens and parasites, but its role in human immune responses remains largely unknown. It is the second most abundant polysaccharide in nature after cellulose and its derivatives today are widely used for medical and industrial purposes. W...

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Autores principales: Jeanette Wagener, R K Subbarao Malireddi, Megan D Lenardon, Martin Köberle, Simon Vautier, Donna M MacCallum, Tilo Biedermann, Martin Schaller, Mihai G Netea, Thirumala-Devi Kanneganti, Gordon D Brown, Alistair J P Brown, Neil A R Gow
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Publicado: Public Library of Science (PLoS) 2014
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Acceso en línea:https://doaj.org/article/896f903ec14a425089cb1524216b009c
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spelling oai:doaj.org-article:896f903ec14a425089cb1524216b009c2021-11-18T06:06:44ZFungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.1553-73661553-737410.1371/journal.ppat.1004050https://doaj.org/article/896f903ec14a425089cb1524216b009c2014-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24722226/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Chitin is an essential structural polysaccharide of fungal pathogens and parasites, but its role in human immune responses remains largely unknown. It is the second most abundant polysaccharide in nature after cellulose and its derivatives today are widely used for medical and industrial purposes. We analysed the immunological properties of purified chitin particles derived from the opportunistic human fungal pathogen Candida albicans, which led to the selective secretion of the anti-inflammatory cytokine IL-10. We identified NOD2, TLR9 and the mannose receptor as essential fungal chitin-recognition receptors for the induction of this response. Chitin reduced LPS-induced inflammation in vivo and may therefore contribute to the resolution of the immune response once the pathogen has been defeated. Fungal chitin also induced eosinophilia in vivo, underpinning its ability to induce asthma. Polymorphisms in the identified chitin receptors, NOD2 and TLR9, predispose individuals to inflammatory conditions and dysregulated expression of chitinases and chitinase-like binding proteins, whose activity is essential to generate IL-10-inducing fungal chitin particles in vitro, have also been linked to inflammatory conditions and asthma. Chitin recognition is therefore critical for immune homeostasis and is likely to have a significant role in infectious and allergic disease.Jeanette WagenerR K Subbarao MalireddiMegan D LenardonMartin KöberleSimon VautierDonna M MacCallumTilo BiedermannMartin SchallerMihai G NeteaThirumala-Devi KannegantiGordon D BrownAlistair J P BrownNeil A R GowPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 4, p e1004050 (2014)
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
Jeanette Wagener
R K Subbarao Malireddi
Megan D Lenardon
Martin Köberle
Simon Vautier
Donna M MacCallum
Tilo Biedermann
Martin Schaller
Mihai G Netea
Thirumala-Devi Kanneganti
Gordon D Brown
Alistair J P Brown
Neil A R Gow
Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
description Chitin is an essential structural polysaccharide of fungal pathogens and parasites, but its role in human immune responses remains largely unknown. It is the second most abundant polysaccharide in nature after cellulose and its derivatives today are widely used for medical and industrial purposes. We analysed the immunological properties of purified chitin particles derived from the opportunistic human fungal pathogen Candida albicans, which led to the selective secretion of the anti-inflammatory cytokine IL-10. We identified NOD2, TLR9 and the mannose receptor as essential fungal chitin-recognition receptors for the induction of this response. Chitin reduced LPS-induced inflammation in vivo and may therefore contribute to the resolution of the immune response once the pathogen has been defeated. Fungal chitin also induced eosinophilia in vivo, underpinning its ability to induce asthma. Polymorphisms in the identified chitin receptors, NOD2 and TLR9, predispose individuals to inflammatory conditions and dysregulated expression of chitinases and chitinase-like binding proteins, whose activity is essential to generate IL-10-inducing fungal chitin particles in vitro, have also been linked to inflammatory conditions and asthma. Chitin recognition is therefore critical for immune homeostasis and is likely to have a significant role in infectious and allergic disease.
format article
author Jeanette Wagener
R K Subbarao Malireddi
Megan D Lenardon
Martin Köberle
Simon Vautier
Donna M MacCallum
Tilo Biedermann
Martin Schaller
Mihai G Netea
Thirumala-Devi Kanneganti
Gordon D Brown
Alistair J P Brown
Neil A R Gow
author_facet Jeanette Wagener
R K Subbarao Malireddi
Megan D Lenardon
Martin Köberle
Simon Vautier
Donna M MacCallum
Tilo Biedermann
Martin Schaller
Mihai G Netea
Thirumala-Devi Kanneganti
Gordon D Brown
Alistair J P Brown
Neil A R Gow
author_sort Jeanette Wagener
title Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
title_short Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
title_full Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
title_fullStr Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
title_full_unstemmed Fungal chitin dampens inflammation through IL-10 induction mediated by NOD2 and TLR9 activation.
title_sort fungal chitin dampens inflammation through il-10 induction mediated by nod2 and tlr9 activation.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/896f903ec14a425089cb1524216b009c
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