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• W1515080523 abstract "Interleukin-1 (IL-1) plays an important role in host defenses against microbial pathogens. Excessive production of this cytokine, however, may be responsible in part for the lethality observed during sepsis. Our studies show that interferon-gamma (IFN-gamma) downregulates lipopolysaccharide (LPS)-induced interleukin-1beta (IL-1beta) transcription in primary macrophages. This phenomenon does not occur in splenocytes or bone marrow-derived macrophages from signal transducer and activator of transcription (Stat1)-deficient mice, suggesting that Stat1, a transcription factor involved in IFN signaling, plays a critical role in this process. Moreover, nitric oxide (NO) was also involved in the downregulation of LPS-induced IL-1 by IFN, as addition of the inducible nitric oxide synthase (iNOS) inhibitor L-N(6)-(1-iminoethyl)lysine (NIL) negated the effect. Kinetic analysis of IL-1 and IFN levels in LPS-treated mice in vivo suggests that IFN-mediated inhibition of IL-1 might be an important negative feedback mechanism for limiting IL-1 generation in vivo." @default.
• W1515080523 created "2016-06-24" @default.
• W1515080523 creator A5003385022 @default.
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• W1515080523 date "2001-07-01" @default.
• W1515080523 modified "2023-09-27" @default.
• W1515080523 title "IFN-<i>γ</i>Inhibits Lipopolysaccharide-Induced Interleukin-1<i>β</i>in Primary Murine Macrophages via a Stat1-Dependent Pathway" @default.
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• W1515080523 doi "https://doi.org/10.1089/10799900152434358" @default.
• W1515080523 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11506742" @default.
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