Aspergillus fumigatus cell wall components differentially modulate host TLR2 and TLR4 responses
Microbes and Infection: a journal on infectious agents and host defenses , Volume 13 - Issue 2 p. 151- 159
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.
|1,4 alpha glucan branching enzyme, Alpha-glucan, Aspergillus, Aspergillus fumigatus, Beta-glucan, Chitin, Galactomannan, Innate immunity, animal experiment, animal model, article, beta glucan, cell wall, chitin, conidium, cytokine production, fungal cell, fungal virulence, galactomannan, immune response, immunomodulation, innate immunity, interleukin 6, male, mixed infection, mouse, nonhuman, pathogenesis, polysaccharide, priority journal, signal transduction, toll like receptor 2, toll like receptor 4|
|Microbes and Infection: a journal on infectious agents and host defenses|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Chai, L.Y.A, Vonk, A.G, Kullberg, B.J, Verweij, P.E, Verschueren, I, van der Meer, J.W.M, … Netea, M.G. (2011). Aspergillus fumigatus cell wall components differentially modulate host TLR2 and TLR4 responses. Microbes and Infection: a journal on infectious agents and host defenses, 13(2), 151–159. doi:10.1016/j.micinf.2010.10.005