Bacterial endotoxin stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms

Journal of Leukocyte Biology - Tập 76 Số 5 - Trang 994-1001 - 2004
Chen Guo-qian1, Jianhua Li2, Mahendar Ochani2, B. Rendon-Mitchell2, Xiaoling Qiang2, Srinivas M. Susarla2, Luis Ulloa2, Huan Yang2, Saijun Fan2, Sanna M. Goyert2, Ping Wang2, Kevin J. Tracey2, Andrew E. Sama1, Haichao Wang2,1
1Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine , Manhasset
2Center of Immunology and Inflammation, North Shore–LIJ Research Institute , Manhasset

Tóm tắt

AbstractBacterial endotoxin [lipopolysaccharide (LPS)] stimulates macrophages to sequentially release early [tumor necrosis factor (TNF)] and late [high mobility group box 1 (HMGB1)] proinflammatory cytokines. The requirement of CD14 and mitogen-activated protein kinases [MAPK; e.g., p38 and extracellular signal-regulated kinase (ERK)1/2] for endotoxin-induced TNF production has been demonstrated previously, but little is known about their involvement in endotoxin-mediated HMGB1 release. Here, we demonstrated that genetic disruption of CD14 expression abrogated LPS-induced TNF production but only partially attenuated LPS-induced HMGB1 release in cultures of primary murine peritoneal macrophages. Pharmacological suppression of p38 or ERK1/2 MAPK with specific inhibitors (SB203580, SB202190, U0126, or PD98059) significantly attenuated LPS-induced TNF production but failed to inhibit LPS-induced HMGB1 release. Consistently, an endogenous, immunosuppressive molecule, spermine, failed to inhibit LPS-induced activation of p38 MAPK and yet, still significantly attenuated LPS-mediated HMGB1 release. Direct suppression of TNF activity with neutralizing antibodies or genetic disruption of TNF expression partially attenuated HMGB1 release from macrophages induced by LPS at lower concentrations (e.g., 10 ng/ml). Taken together, these data suggest that LPS stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms.

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Journal of Leukocyte Biology

Tập 76 Số 5

994-1001

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