Department of Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Microbes Infect. 2011 Feb;13(2):151-9. doi: 10.1016/j.micinf.2010.10.005. Epub 2010 Nov 4.
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.
烟曲霉分生孢子通过调节 Toll 样受体 (TLR)2 和 TLR4 信号来减弱宿主的促炎反应，但介导这种效应的确切机制尚不清楚。在本研究中，研究了负责调节宿主产生促炎反应能力的曲霉细胞壁多糖成分的作用。曲霉细胞壁级分及其主要成分在调节宿主 TLR 介导体细胞因子 (IL)-6 产生方面表现出不同的能力。β-葡聚糖特异性抑制 TLR4 诱导的反应，而α-葡聚糖抑制通过 TLR2 和 TLR4 刺激诱导的 IL-6。半乳甘露聚糖减弱 TLR4 介导的反应，而其对 TLR2 信号的抑制作用有限。另一方面，几丁质没有显著的免疫调节能力。真菌细胞壁改变病原体免疫特征的能力可能与其毒力和合并感染的发病机制有关。
