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• W1545375815 endingPage "2612" @default.
• W1545375815 startingPage "2606" @default.
• W1545375815 abstract "Abstract G-CSF is a hemopoietic growth factor involved in granulocytic differentiation of progenitor cells. In this study, we investigated the effects of PGE2 on G-CSF production in murine peritoneal neutrophils in vitro and in vivo. PGE2 augmented LPS-primed G-CSF release from peritoneal neutrophils. This augmentation was mimicked by a type E prostanoid receptor (EP)2-selective agonist but not by other EP-specific agonists. Indeed, the effect of PGE2 on G-CSF release was abolished in neutrophils isolated from EP2-deficient mice. PGE2 and an EP2 agonist have the ability to stimulate G-CSF gene expression even in the absence of LPS. In the casein-induced peritonitis model, the appearance of G-CSF in the casein-injected peritoneal cavity associated well with the timing of neutrophil infiltration as well as PGE2 levels in exudates, with a peak value at 6 h postinjection. Inhibition of endogenous PG synthesis by indomethacin resulted in a marked decrease in G-CSF content and neutrophil number in the peritoneal cavity. Moreover, EP2-deficient mice exhibited a strikingly reduced G-CSF content in peritoneal exudates with comparable responses in neutrophil migration and local PGE2 production at 6 h postinjection. These results suggest that the PGE2-EP2 system contributes to the local production of G-CSF during acute inflammation." @default.
• W1545375815 created "2016-06-24" @default.
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• W1545375815 date "2005-08-15" @default.
• W1545375815 modified "2023-10-17" @default.
• W1545375815 title "Prostaglandin E2 Stimulates Granulocyte Colony-Stimulating Factor Production via the Prostanoid EP2 Receptor in Mouse Peritoneal Neutrophils" @default.
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• W1545375815 doi "https://doi.org/10.4049/jimmunol.175.4.2606" @default.
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