Aspergillus fumigatus cell wall components differentially modulate host TLR2 and TLR4 responses

被引:72
|
作者
Chai, Louis Y. A. [1 ,2 ,3 ]
Vonk, Alieke G. [4 ]
Kullberg, Bart Jan [1 ,2 ]
Verweij, Paul E. [2 ,5 ]
Verschueren, Ineke [1 ,2 ]
van der Meer, Jos W. M. [1 ,2 ]
Joosten, Leo A. B. [1 ,2 ]
Latge, Jean-Paul [6 ]
Netea, Mihai G. [1 ,2 ]
机构
[1] Radboud Univ Nijmegen, Med Ctr, Dept Med, NL-6525 GA Nijmegen, Netherlands
[2] Nijmegen Inst Infect Inflammat & Immun N4i, NL-6525 GA Nijmegen, Netherlands
[3] Natl Univ Hlth Syst, Dept Med, Singapore 119228, Singapore
[4] Univ Med Ctr Rotterdam, Erasmus MC, Dept Med Microbiol & Infect Dis, NL-3015 CE Rotterdam, Netherlands
[5] Radboud Univ Nijmegen, Med Ctr, Dept Microbiol, NL-6525 GA Nijmegen, Netherlands
[6] Inst Pasteur, Unite Aspergillus, F-75015 Paris, France
基金
英国医学研究理事会;
关键词
Innate immunity; Beta-glucan; Chitin; Galactomannan; Alpha-glucan; BETA-GLUCAN RECEPTOR; CANDIDA-ALBICANS; CYTOKINE RELEASE; HUMAN MONOCYTES; FUNGAL CELL; IMMUNITY; DECTIN-1; INNATE; RECOGNITION; PROTEINS;
D O I
10.1016/j.micinf.2010.10.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Aspergillus fumigatus conidia attenuates host proinflammatory responses through modulation of Toll-like receptor (TLR)2 and TLR4 signaling, but file 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. (C) 2010 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:151 / 159
页数:9
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