Abstract |
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.
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Authors | Louis Y A Chai, Bart Jan Kullberg, Alieke G Vonk, Adilia Warris, Alessandra Cambi, Jean-Paul Latgé, Leo A B Joosten, Jos W M van der Meer, Mihai G Netea |
Journal | Infection and immunity
(Infect Immun)
Vol. 77
Issue 5
Pg. 2184-92
(May 2009)
ISSN: 1098-5522 [Electronic] United States |
PMID | 19204090
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-1beta
- Interleukin-6
- TLR4 protein, human
- Toll-Like Receptor 2
- Toll-Like Receptor 4
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Topics |
- Aspergillus fumigatus
(immunology)
- Humans
- Hyphae
(immunology)
- Immune Tolerance
- Interleukin-1beta
(antagonists & inhibitors, biosynthesis)
- Interleukin-6
(antagonists & inhibitors, biosynthesis)
- Spores, Fungal
(immunology)
- Toll-Like Receptor 2
(immunology)
- Toll-Like Receptor 4
(immunology)
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