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• W1996042312 startingPage "L374" @default.
• W1996042312 abstract "Cystic fibrosis (CF) airway epithelial cells are more susceptible to viral infection due to impairment of the innate host defense pathway of nitric oxide (NO). NO synthase-2 (NOS2) expression is absent, and signal transducer and activator of transcription (STAT) 1 activation is reduced in CF. We hypothesized that the IFN-γ signaling pathway, which leads to NOS2 gene induction in CF airway epithelial cells, is defective. In contrast to a lack of NOS2 induction, the major histocompatibility complex class 2, an IFN-γ-regulated delayed-responsive gene, is similarly induced in CF and non-CF airway epithelial (NL) cells, suggesting an NOS2-specific defect in the IFN-γ signaling pathway. STAT1 and activator protein-1, both required for NOS2 gene expression, interact normally in CF cells. Protein inhibitor of activated STAT1 is not increased in CF cells. IFN-γ induces NOS2 expression in airway epithelial cells through an autocrine mechanism involving synthesis and secretion of IFN-γ-inducible mediator(s), which activates STAT1. Here, CF cells secrete IFN-γ-inducible factor(s), which stimulate NOS2 expression in NL cells, but not in CF cells. In contrast, IFN-γ-inducible factor(s) similarly inhibit virus in CF and NL cells. Thus autocrine activation of NOS2 is defective in CF cells, but IFN-γ induction of antiviral host defense is intact." @default.
• W1996042312 created "2016-06-24" @default.
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• W1996042312 date "2004-08-01" @default.
• W1996042312 modified "2023-09-23" @default.
• W1996042312 title "Impaired nitric oxide synthase-2 signaling pathway in cystic fibrosis airway epithelium" @default.
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• W1996042312 doi "https://doi.org/10.1152/ajplung.00039.2004" @default.
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