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Am J Physiol Cell Physiol (January 21, 2004). doi:10.1152/ajpcell.00387.2003
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Submitted on September 11, 2003
Accepted on January 16, 2004

Selective activation of STAT3 in human monocytes stimulated by G-CSF: implication in G-CSF-mediated inhibition of LPS-induced TNF{alpha} production

SAORI NISHIKI1, FUMIHIKO HATO1, NORIKO KAMATA1, ERINA SAKAMOTO1, TARO HASEGAWA1, AKIKO KIMURA-ETO1, MASAYUKI HINO1, and SEIICHI KITAGAWA1*

1 Department of Physiology, Osaka City University, Osaka, Japan

* To whom correspondence should be addressed. E-mail: kitagawas{at}med.osaka-cu.ac.jp.

Lipopolysaccharide (LPS) induced tumor necrosis factor-{alpha} (TNF{alpha}) production in human monocytes, which was dependent on activation of extracellular-signal regulated kinase (ERK), p38, c-Jun N-terminal kinase (JNK) and NF-{kappa}B. LPS-induced TNF{alpha} production was inhibited by granulocyte colony-stimulating factor (G-CSF) and interleukin-10 (IL-10). G-CSF, like IL-10, exerted the inhibitory effect even when simultaneously added with LPS. Among the signaling pathways, signal transducer and activator of transcription 3 (STAT3) was selectively activated in monocytes stimulated by G-CSF or IL-10. G-CSF-mediated inhibition of LPS-induced TNF{alpha} production as well as G-CSF-induced STAT3 phosphorylation and suppressor of cytokine signaling 3 (SOCS3) mRNA expression was prevented by pretreatment of monocytes with AG490, an inhibitor of Janus kinase 2. G-CSF did not affect LPS-induced activation of ERK, p38, JNK and NF-{kappa}B, indicating that G-CSF affects the pathway downstream or independent of these signaling molecules. G-CSF-induced, but not IL-10-induced, STAT3 phosphorylation was attenuated in the presence of LPS. These findings suggest that G-CSF, like IL-10, inhibits LPS-induced TNF{alpha} production in human monocytes through selective activation of STAT3 and the immunomodulation observed in vivo by G-CSF administration may be partly ascribed to the direct effect of G-CSF on monocyte functions.




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