Basic Research
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 28, 2005; 11(32): 4979-4985
Published online Aug 28, 2005. doi: 10.3748/wjg.v11.i32.4979
CXCL16 participates in pathogenesis of immunological liver injury by regulating T lymphocyte infiltration in liver tissue
Huan-Bin Xu, Yan-Ping Gong, Jin Cheng, Yi-Wei Chu, Si-Dong Xiong
Huan-Bin Xu, Yan-Ping Gong, Jin Cheng, Yi-Wei Chu, Si-Dong Xiong, Department of Immunology and Key Laboratory of Molecular Medicine of Ministry of Education, Shanghai Medical College of Fudan University; Immunology Division, E-Institute of Shanghai Universities, Shanghai 200032, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 30230320, National Science Fund for Distinguished Young Scholars from NSFC, No. 39925031, National High Technology Research and Development Program of China, 863 grant 2004 AA215242, Major State Basic Research Development Program of China, No. 2001CB510005 and partially by E-Institute of Shanghai Universities
Correspondence to: Dr. Si-Dong Xiong, Department of Immunology, Shanghai Medical College of Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. sdxiong@shmu.edu.cn
Telephone: +86-21-54237749 Fax: +86-21-54237749
Received: October 21, 2004
Revised: December 23, 2004
Accepted: December 26, 2004
Published online: August 28, 2005
Abstract

AIM: To investigate the role of CXCL16 in the pathogenesis of immunological liver injury and to explore the possible mechanism of T lymphocyte infiltration regulated by CXCL16.

METHODS: Immunological liver injury in murine model was induced by Bacille Calmette-Guerin and lipopolysaccharide. Expression pattern and distribution of CXCL16 were examined by real-time quantitative RT-PCR and immunohistochemical analysis. Anti-CXCL16 antibody was administrated in vivo to investigate its effect on T-cell recruitment and acute hepatic necrosis. The survival of murine model was also evaluated.

RESULTS: The murine immunological liver injury model was successfully established. CXCL16 expression increased and predominantly distributed in periportal areas and vascular endothelia in injured liver tissues. Administration of anti-CXCL16 Ab protected the mice from death and acute liver damage. Approximately 70% of the mice survived for 72 h in the anti-CXCL16 Ab treatment group, whereas 80% died within 72 h in control Ab group. The number of liver-infiltrating T lymphocytes was significantly reduced from 1.01×107 to 3.52×106/liver, compared with control Ab treatment.

CONCLUSION: CXCL16 is involved in immunological liver injury by regulating T lymphocyte infiltration in liver tissue.

Keywords: Chemokines; CXCL16; T lymphocytes; Infiltration; Immunological liver injury