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Acta Biochimica et Biophysica Sinica 2009 41(2):171-177; doi:10.1093/abbs/gmn020
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Different effect of glutamine on macrophage tumor necrosis factor-alpha release and heat shock protein 72 expression in vitro and in vivo

Mengfan Liang1,{dagger}, Xuemin Wang1,{dagger}, Yuan Yuan1, Quanhong Zhou1, Chuanyao Tong2 and Wei Jiang1,*

1 Department of Anesthesiology/Intensive Care Unit, 6th Municipal Hospital, Medical College of Shanghai Jiao Tong University, Shanghai, China
2 Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina, USA

* Correspondence address. Tel: +86-21-64086795; Fax: +86-21-64368920; E-mail: jiangw{at}sjtu.edu.cn


  Abstract

Macrophage plays a vital role in sepsis. However, the modulatory effect of glutamine (Gln) on macrophage/monocyte-mediate cytokines release is still controversial. Thus, we investigated the effect of Gln on macrophage tumor necrosis factor (TNF)-{alpha} release and heat shock protein (HSP) 72 expression in vivo and in vitro. Data from our study indicated that the increase of HSP72 expression was significant at 8 mM of Gln 4 h after lipopolysaccharide (LPS) stimulation and became independent of Gln concentrations at 24 h, whereas TNF-{alpha} release was dose- and time-dependent on Gln. Heat stress (HS) induced more HSP72 and less TNF-{alpha} production compared with the non-HS group. However, the production of TNF-{alpha} in cells pretreated with HS was increased with increasing concentrations of Gln. Treatment with various concentrations of Gln for 1 h and then 0.5 mM Gln for 4 h led to an increase in HSP72 expression, but not in TNF-{alpha} production. In sepsis model mice, Gln treatment led to a significantly lower intracellular TNF-{alpha} level and an increase in HSP72 expression in mouse peritoneal macrophages. Our results demonstrate that Gln directly increases TNF-{alpha} release of LPS-stimulated RAW264.7 macrophages in a dose-dependent manner, and also decreases mouse peritoneal macrophages TNF-{alpha} release in the sepsis model. Taken together, our data suggest that there may be more additional pathways by which Gln modulates cytokine production besides HSP72 expression in macrophage during sepsis.

Keywords    glutamine; heat shock protein 72; tumor necrosis factor-alpha; macrophage

Received: September 27, 2008; Accepted: November 19, 2008

{dagger} These authors contributed equally to this work


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