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• W2020148236 abstract "Lipopolysaccharide (LPS) induces a marked delay in human neutrophil apoptosis that is reversed by the anti-inflammatory cytokine IL-10. The effect of IL-10 is specific since other agents that delay neutrophil apoptosis are not affected. To investigate mechanisms underlying the actions of IL-10, we examined signaling pathways activated by LPS per se and in response to IL-10. The MAPK kinase (MEK) 1 inhibitor PD098059, the protein kinase C (PKC) inhibitor Ro31,8220, and the phosphatidylinositol-3 kinase (PI3-K) inhibitor LY294002 all partially reversed LPS-mediated retardation of neutrophil apoptosis, but the p38 MAPK inhibitor SB203850 did not. LPS activates the transcription factor NF-kappaB, however, IL-10 did not affect the ability of LPS to activate NF-kappaB as assessed by IkappaB-alpha proteolysis. Although IL-10 did not alter activation of ERK by GM-CSF or TNF-alpha, it did inhibit activation induced by LPS. Thus our data illustrate that LPS-induced neutrophil survival is regulated by the MAPK, PKC and PI3-K pathways as well as NF-kappaB, and can be reversed by IL-10, through a mechanism involving inhibition of ERK activation. Because of the specific nature of this inhibition, we conclude that IL-10 interferes with an ERK activation pathway, which is not involved in GM-CSF or TNF-alpha signaling." @default.
• W2020148236 created "2016-06-24" @default.
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• W2020148236 date "2005-09-01" @default.
• W2020148236 modified "2023-09-25" @default.
• W2020148236 title "Interleukin-10 inhibits lipopolysaccharide-induced survival and extracellular signal-regulated kinase activation in human neutrophils" @default.
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• W2020148236 doi "https://doi.org/10.1002/eji.200425561" @default.
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