Chai Louis Y A, Kullberg Bart Jan, Vonk Alieke G, Warris Adilia, Cambi Alessandra, Latgé Jean-Paul, Joosten Leo A B, van der Meer Jos W M, Netea Mihai G
Department of Medicine (463), Radboud University Nijmegen Medical Center, P.O. Box 9101, Geert Grootplein 8, 6525 GA Nijmegen, The Netherlands.
Infect Immun. 2009 May;77(5):2184-92. doi: 10.1128/IAI.01455-08. Epub 2009 Feb 9.
Toll-like receptor (TLR)-based signaling pathways in the host may be modulated by pathogens during the course of infection. We describe a novel immunomodulatory mechanism in which Aspergillus fumigatus conidia induce attenuation of TLR2- and TLR4-mediated interleukin (IL)-6 and IL-1beta proinflammatory responses in human mononuclear cells with suppression of IL-1beta mRNA transcription. Background TLR2 and TLR4 mRNA transcription was not influenced. A. fumigatus conidia induced TLR2 internalization and uptake into the phagosome with a resultant decrease in surface receptor expression. A. fumigatus hyphae, on the other hand, selectively downregulated the TLR4-mediated response. These novel immunosuppressive effects may facilitate the invasiveness of A. fumigatus.
在感染过程中，宿主基于Toll样受体（TLR）的信号通路可能受到病原体的调节。我们描述了一种新的免疫调节机制，其中烟曲霉分生孢子可诱导人单核细胞中TLR2和TLR4介导的白细胞介素（IL）-6和IL-1β促炎反应减弱，并抑制IL-1β mRNA转录。背景TLR2和TLR4 mRNA转录不受影响。烟曲霉分生孢子诱导TLR2内化并被摄取到吞噬体中，导致表面受体表达下降。另一方面，烟曲霉菌丝选择性地下调TLR4介导的反应。这些新的免疫抑制作用可能有助于烟曲霉的侵袭性。
