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- W2025648442 abstract "Severe respiratory syncytial virus (RSV)-induced bronchiolitis has been associated with a mixed “Th1” and “Th2” cytokine storm. We hypothesized that differentiation of “alternatively activated” macrophages (AA-Mφ) would mediate the resolution of RSV-induced lung injury. RSV induced interleukin (IL)-4 and IL-13 by murine lung and peritoneal macrophages, IL-4Rα/STAT6-dependent AA-Mφ differentiation, and significantly enhanced inflammation in the lungs of IL-4Rα−/− mice. Adoptive transfer of wildtype macrophages to IL-4Rα−/− mice restored RSV-inducible AA-Mφ phenotype and diminished lung pathology. RSV-infected Toll-like receptor (TLR)4−/− and interferon (IFN)-β−/− macrophages and mice also failed to express AA-Mφ markers, but exhibited sustained proinflammatory cytokine production (e.g., IL-12) in vitro and in vivo and epithelial damage in vivo. TLR4 signaling is required for peroxisome proliferator-activated receptorγ expression, a DNA-binding protein that induces AA-Mφ genes, whereas IFN-β regulates IL-4, IL-13, IL-4Rα, and IL-10 expression in response to RSV. RSV-infected cotton rats treated with a cyclooxygenase-2 inhibitor increased expression of lung AA-Mφ. These data suggest new treatment strategies for RSV that promote AA-Mφ differentiation." @default.
- W2025648442 created "2016-06-24" @default.
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- W2025648442 date "2010-03-10" @default.
- W2025648442 modified "2023-10-14" @default.
- W2025648442 title "Control of RSV-induced lung injury by alternatively activated macrophages is IL-4Rα-, TLR4-, and IFN-β-dependent" @default.
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- W2025648442 doi "https://doi.org/10.1038/mi.2010.6" @default.
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