IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2

Candida albicans is a fungus that is an opportunistic pathogen of humans. Normally, C. albicans exists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage to C. albicans. IL-34 is a recently...

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Main Authors: Rong Xu, Hong-Fan Sun, David W. Williams, Adam V. Jones, Ali Al-Hussaini, Bing Song, Xiao-Qing Wei
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2015/328146
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author Rong Xu
Hong-Fan Sun
David W. Williams
Adam V. Jones
Ali Al-Hussaini
Bing Song
Xiao-Qing Wei
author_facet Rong Xu
Hong-Fan Sun
David W. Williams
Adam V. Jones
Ali Al-Hussaini
Bing Song
Xiao-Qing Wei
author_sort Rong Xu
collection DOAJ
description Candida albicans is a fungus that is an opportunistic pathogen of humans. Normally, C. albicans exists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage to C. albicans. IL-34 is a recently discovered cytokine, constitutively expressed by keratinocytes in the skin. IL-34 binds to the receptor of M-CSF, thereby stimulating tissue macrophage maturation and differentiation. Resident macrophages exhibit phenotypic plasticity and may transform into inflammatory M1 macrophages for immunity or anti-inflammatory M2 macrophages for tissue repair. M1 macrophages produce higher levels of inflammatory cytokines such as TNFα in response to C. albicans stimulation. In this study, it was demonstrated that IL-34 attenuated TNFα production by M1 macrophages challenged with heat killed Candida (HKC). The molecular mechanism of IL-34 mediated suppression of HKC induced TNFα production by M1 macrophages was by the inhibition of M1 macrophage expression of key C. albicans pattern recognition receptors (PPRs), namely, Toll-like receptor (TLR) 2 and Dectin-1. The results of this study indicated that constitutive IL-34 expressed by skin keratinocytes might suppress resident macrophage responses to C. albicans colonisation by maintaining low levels TLR2 and Dectin-1 expression by macrophages.
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language English
publishDate 2015-01-01
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spelling doaj-art-f9e740e83c7f4c0bb054c6a4a705d7c82025-02-03T05:50:57ZengWileyJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/328146328146IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2Rong Xu0Hong-Fan Sun1David W. Williams2Adam V. Jones3Ali Al-Hussaini4Bing Song5Xiao-Qing Wei6Tissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKTianjin Key Laboratory of Biomaterial Research, Institute of Biomedical Engineering, Chinese Academy of Medical Science, Tianjin 300192, ChinaTissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKTissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKTissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKTissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKTissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UKCandida albicans is a fungus that is an opportunistic pathogen of humans. Normally, C. albicans exists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage to C. albicans. IL-34 is a recently discovered cytokine, constitutively expressed by keratinocytes in the skin. IL-34 binds to the receptor of M-CSF, thereby stimulating tissue macrophage maturation and differentiation. Resident macrophages exhibit phenotypic plasticity and may transform into inflammatory M1 macrophages for immunity or anti-inflammatory M2 macrophages for tissue repair. M1 macrophages produce higher levels of inflammatory cytokines such as TNFα in response to C. albicans stimulation. In this study, it was demonstrated that IL-34 attenuated TNFα production by M1 macrophages challenged with heat killed Candida (HKC). The molecular mechanism of IL-34 mediated suppression of HKC induced TNFα production by M1 macrophages was by the inhibition of M1 macrophage expression of key C. albicans pattern recognition receptors (PPRs), namely, Toll-like receptor (TLR) 2 and Dectin-1. The results of this study indicated that constitutive IL-34 expressed by skin keratinocytes might suppress resident macrophage responses to C. albicans colonisation by maintaining low levels TLR2 and Dectin-1 expression by macrophages.http://dx.doi.org/10.1155/2015/328146
spellingShingle Rong Xu
Hong-Fan Sun
David W. Williams
Adam V. Jones
Ali Al-Hussaini
Bing Song
Xiao-Qing Wei
IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
Journal of Immunology Research
title IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
title_full IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
title_fullStr IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
title_full_unstemmed IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
title_short IL-34 Suppresses Candida albicans Induced TNFα Production in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2
title_sort il 34 suppresses candida albicans induced tnfα production in m1 macrophages by downregulating expression of dectin 1 and tlr2
url http://dx.doi.org/10.1155/2015/328146
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