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• W2023385268 abstract "Exposure to environmental tobacco smoke (ETS) is associated with an increase in the frequency and severity of respiratory infections, including bronchiolitis, a clinical syndrome of infancy caused by viruses such as respiratory syncytial virus (RSV). The mechanisms by which ETS increases the risk of viral respiratory infections are largely unknown. A major effector integrating early antiviral and immunostimulatory activities is interferon-α (IFN-α), which is highly produced by plasmacytoid dendritic cells (pDC). In this work, we determined the effect of cigarette smoke extract (CSE) on human pDC immunity in response to a respiratory viral infection. We found that CSE inhibited RSV-induced IFN-α in pDC as well as the release of IL-1β, IL-10 and CXCL10. However, the production of additional cytokines and chemokines such as IL-6, TNF-α, CCL2, CCL3, CCL5 and CXCL8 was not altered. Quantitative RT-PCR analysis indicated that CSE decreased the expression of toll-like receptor (TLR)-7 and interferon regulatory factor (IRF)-7 in RSV-infected pDC. Furthermore, determination of IRF-7 phosphorylation by flow cytometry showed that CSE prevented IRF-7 activation. These data provide evidence that cigarette smoke suppresses key pDC functions upon viral infection by a mechanism that involves downregulation of TLR7 expression and decreased activation of IRF-7." @default.
• W2023385268 created "2016-06-24" @default.
• W2023385268 creator A5053778355 @default.
• W2023385268 creator A5080946365 @default.
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• W2023385268 date "2011-08-01" @default.
• W2023385268 modified "2023-09-23" @default.
• W2023385268 title "Cigarette smoke suppresses TLR-7 stimulation in response to virus infection in plasmacytoid dendritic cells" @default.
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• W2023385268 doi "https://doi.org/10.1016/j.tiv.2011.03.011" @default.
• W2023385268 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21435390" @default.
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