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• W2105227585 startingPage "3354" @default.
• W2105227585 abstract "Abstract Inflammation is counterbalanced by anti-inflammatory cytokines such as IL-10, in which Stat3 mediates the signaling pathway. In this study, we demonstrate that resident macrophages, but not other cell types, are important targets of IL-10 in a murine model of acute peritonitis. Injection of thioglycollate i.p. induced a considerable number of neutrophils and macrophages in the peritoneum, which was significantly augmented in mice with a cell-type specific disruption of the Stat3 gene in macrophages and neutrophils (LysMcre/Stat3flox/− mice). The augmented leukocyte infiltration was accompanied by increased peritoneal levels of TNF-α, MIP-2, KC chemokine (KC), and MCP-1/CCL2. Stat3 was tyrosine phosphorylated in peritoneal resident macrophages as well as infiltrating leukocytes in the littermate controls, suggesting that Stat3 in either or both of these cells might play a regulatory role in inflammation. The peritoneal levels of TNF-α, MIP-2, KC, and MCP-1 were similarly elevated in LysMcre/Stat3flox/− mice rendered leukopenic by cyclophosphamide treatment as compared with the controls. Adoptive transfer of resident macrophages from LysMcre/Stat3flox/− mice into the control littermates resulted in increases in the peritoneal level of TNF-α, MIP-2, KC, and MCP-1 after i.p. injection of thioglycollate. Under these conditions, control littermates harboring LysMcre/Stat3flox/− macrophages exhibited an augmented leukocyte infiltration relative to those received control macrophages. Taken together, these data provide evidence that resident macrophages, but not other cell types, play a regulatory role in inflammation through a Stat3 signaling pathway. Stat3 in resident macrophages appears to function as a repressor protein in this model of acute inflammation." @default.
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• W2105227585 date "2005-09-01" @default.
• W2105227585 modified "2023-09-23" @default.
• W2105227585 title "Stat3 in Resident Macrophages as a Repressor Protein of Inflammatory Response" @default.
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• W2105227585 doi "https://doi.org/10.4049/jimmunol.175.5.3354" @default.
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