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Prostaglandin E₂ Stimulates Granulocyte Colony-Stimulating Factor Production via the Prostanoid EP2 Receptor in Mouse Peritoneal Neutrophils ¹

Yukihiko Sugimoto^2,*, Yoko Fukada^2,*, Daisuke Mori^2,*, Satoshi Tanaka^*, Hana Yamane^*, Yasushi Okuno, Katsuya Deai^*, Soken Tsuchiya^*, Gozoh Tsujimoto and Atsushi Ichikawa^3,*,

^* Department of Physiological Chemistry and Department of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan; and School of Pharmaceutical Sciences, Mukogawa Women’s University, Hyogo, Japan

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.

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