Recognition and Blocking of Innate Immunity Cells by Candida albicans Chitin

Chitin is a skeletal cell wall polysaccharide of the inner cell wall of fungal pathogens. As yet, little about its role during fungus-host immune cell interactions is known. We show here that ultrapurified chitin from Candida albicans cell walls did not stimulate cytokine production directly but blo...

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Bibliographic Details
Published in:Infection and Immunity 2011-05, Vol.79 (5), p.1961-1970
Main Authors: Mora-Montes, Héctor M, Netea, Mihai G, Ferwerda, Gerben, Lenardon, Megan D, Brown, Gordon D, Mistry, Anita R, Kullberg, Bart Jan, O'Callaghan, Chris A, Sheth, Chirag C, Odds, Frank C, Brown, Alistair J.P, Munro, Carol A, Gow, Neil A.R, Deepe, G.S. Jr
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Candida albicans
Candida albicans - immunology
Candidiasis - immunology
cell walls
chitin
Chitin - immunology
cytokines
Cytokines - biosynthesis
Cytokines - immunology
Fundamental and applied biological sciences. Psychology
Fungal and Parasitic Infections
fungi
Host-Parasite Interactions - immunology
Humans
Immunity, Innate - immunology
innate immunity
lectins
Lectins, C-Type
Leukocytes, Mononuclear - immunology
lipopolysaccharides
macrophages
Macrophages - immunology
Membrane Proteins - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Microbiology
Microscopy, Fluorescence
Miscellaneous
mononuclear leukocytes
Mycology
Nerve Tissue Proteins - immunology
pathogens
receptors
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Description
Summary:Chitin is a skeletal cell wall polysaccharide of the inner cell wall of fungal pathogens. As yet, little about its role during fungus-host immune cell interactions is known. We show here that ultrapurified chitin from Candida albicans cell walls did not stimulate cytokine production directly but blocked the recognition of C. albicans by human peripheral blood mononuclear cells (PBMCs) and murine macrophages, leading to significant reductions in cytokine production. Chitin did not affect the induction of cytokines stimulated by bacterial cells or lipopolysaccharide (LPS), indicating that blocking was not due to steric masking of specific receptors. Toll-like receptor 2 (TLR2), TLR4, and Mincle (the macrophage-inducible C-type lectin) were not required for interactions with chitin. Dectin-1 was required for immune blocking but did not bind chitin directly. Cytokine stimulation was significantly reduced upon stimulation of PBMCs with heat-killed chitin-deficient C. albicans cells but not with live cells. Therefore, chitin is normally not exposed to cells of the innate immune system but is capable of influencing immune recognition by blocking dectin-1-mediated engagement with fungal cell walls.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.01282-10