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Title: Aspergillus fumigatus cell wall components differentially modulate host TLR2 and TLR4 responses
Author(s): Chai, L. ; Vonk, A.G. ; Kullberg, B.J. ; Verweij, P.E. ; Verschueren, I. ; Meer, J.W.M. van der ; Joosten, L.A.B. ; Latge, J.P.; Netea, M.G.
Publication year: 2011
Source: Microbes and Infection, vol. 13, iss. 2, (2011), pp. 151-159
ISSN: 1286-4579
DOI: http://dx.doi.org/10.1016/j.micinf.2010.10.005
Publication type: Article / Letter to editor

Please use this identifier to cite or link to this item : http://hdl.handle.net/2066/95652   http://hdl.handle.net/2066/95652

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Subject: N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity
N4i 2: Invasive mycoses and compromised host NCMLS 1: Infection and autoimmunity
Organization: Internal Medicine
Medical Microbiology
Journal title:
Microbes and Infection
Volume: vol. 13
Issue: iss. 2
Page start: p. 151
Page end: p. 159
Abstract:
Aspergillus fumigatus conidia attenuates host proinflammatory responses through modulation of Toll-like receptor (TLR)2 and TLR4 signaling, but the precise mechanisms that mediate this effect are not known. In the present study, the role of the Aspergillus cell wall polysaccharide constituents responsible for the modulation of host capability to mount a proinflammatory response was studied. Aspergillus cell wall fractions and its major components showed differential capabilities in modulating host TLR-mediated interleukin (IL)-6 production. Beta-glucan specifically suppressed TLR4-induced response, while alpha-glucan inhibited IL-6 induced through TLR2- and TLR4-stimulation. Galactomannan diminished TLR4-mediated response, while its inhibitory effects on TLR2-signaling were limited. Chitin, on the other hand, did not have significant immunomodulatory capability. The ability of the fungal cell wall to alter the immune signature of the pathogen may contribute to its virulence and the pathogenesis of co-infection.

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