Recognition and blocking of innate immunity cells by Candida albicans chitin
Publication year
2011Source
Infection and Immunity, 79, 5, (2011), pp. 1961-70ISSN
Publication type
Article / Letter to editor
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Organization
Internal Medicine
Paediatrics - OUD tm 2017
Laboratory of Genetic, Endocrine and Metabolic Diseases
Journal title
Infection and Immunity
Volume
vol. 79
Issue
iss. 5
Page start
p. 1961
Page end
p. 70
Subject
N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity; N4i 2: Invasive mycoses and compromised host NCMLS 1: Infection and autoimmunityAbstract
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.
This item appears in the following Collection(s)
- Academic publications [238426]
- Electronic publications [122508]
- Faculty of Medical Sciences [90358]
- Open Access publications [97504]
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