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Infection and Immunity, July 2005, p. 4007-4016, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4007-4016.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Involvement of Up-Regulated CXC Chemokine Ligand 16/Scavenger Receptor That Binds Phosphatidylserine and Oxidized Lipoprotein in Endotoxin-Induced Lethal Liver Injury via Regulation of T-Cell Recruitment and Adhesion

Huanbin Xu,¹ Wei Xu,¹ Yiwei Chu,¹ Yanping Gong,¹ Zhenggang Jiang,¹ and Sidong Xiong^1,2*

Department of Immunology and Key Laboratory of Molecular Medicine of Ministry of Education, Shanghai Medical College of Fudan University, and,¹ Immunology Division, E-Institute of Shanghai Universities, Shanghai 200032, People’s Republic of China²

Received 28 October 2004/ Returned for modification 15 December 2004/ Accepted 27 February 2005

A murine model of endotoxin-induced lethal liver injury induced by Mycobacterium bovis BCG plus lipopolysaccharide (LPS) has been widely accepted and used. It has been reported that T cells play an important role in the pathogenesis of liver damage in this model. However, the precise mechanisms involved in regulation of the trafficking of effector T cells need to be elucidated. In the present study, we first reported that CXCL16/SR-PSOX (CXC chemokine ligand 16/scavenger receptor that binds phosphatidylserine and oxidized lipoprotein), a chemokine containing both membrane-anchored and soluble forms, was strongly up-regulated and predominantly distributed in the vascular endothelium in the injured liver tissue in the model. The secretory and membrane-anchored CXCL16/SR-PSOX functioned as a chemokine and an adhesive molecule, respectively, to attract T cells to a tumor necrosis factor alpha-activated endothelial cell line (SVEC) in vitro. To further identify the pathophysiological roles of CXCL16/SR-PSOX in the liver injury, the anti-CXCL16 antibody was administered to the BCG-primed mice before LPS challenge in vivo. Significant protection effects were observed with 70% of mice regarding lethality, the massive necrosis in the liver was reduced, and the intrahepatic infiltrating T cells were significantly inhibited. Taken together, these findings strongly suggest that functional CXCL16/SR-PSOX, as both a chemokine and an adhesion molecule, may be involved in the pathogenesis of the endotoxin-induced lethal liver injury via recruitment and adhesion of activated T cells to the vascular endothelium.

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* Corresponding author. Mailing address: Department of Immunology, Shanghai Medical College of Fudan University, 138 Yi Xue Yuan Road, Shanghai 200032, People’s Republic of China. Phone and fax: 86 21 54237749. E-mail: sdxiongfd{at}126.com.

Editor: J. L. Flynn

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Infection and Immunity, July 2005, p. 4007-4016, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4007-4016.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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