Toll-like receptor 2 contributes to liver injury by salmonella infection through Fas ligand expression on NKT cells in mice

被引:43
作者
Shimizu, H
Matsuguchi, T
Fukuda, Y
Nakano, I
Hayakawa, T
Takeuchi, O
Akira, S
Umemura, M
Suda, T
Yoshikai, Y
机构
[1] Nagoya Univ, Sch Med, Lab Host Def & Germfree Life, Dis Mechanism & Control Res Inst,Showa Ku, Nagoya, Aichi 4668550, Japan
[2] Nagoya Univ, Sch Med, Dept Internal Med 2, Nagoya, Aichi 4668550, Japan
[3] Osaka Univ, Dept Host Def, Microbial Dis Res Inst, Osaka, Japan
[4] Kanazawa Univ, Ctr Dev Mol Target Drugs, Inst Canc Res, Kanazawa, Ishikawa 920, Japan
关键词
D O I
10.1053/gast.2002.36006
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Toll-like receptors (TLRs) for bacterial constitutes are expressed not only by phagocytes but also by some subsets of T cells. We previously reported that natural killer T cells (NKT cells) play an, important role in liver injury induced by Salmonella infection. In the present study, we investigated whether TLRs on NKT cells are involved in Salmonella-induced liver injury. Methods: Gene express! on of TLR2 was examined in sorted natural killer, NKT, and T cells from livers of naive mice by the reverse-transcription polymerase chain reaction method. Serum alanine aminotransferase level and FasL expression on liver lymphocytes were examined in TLR2-deficient (TLR2(-/-)) and FasL-deficient gld/gld mice before and after intraperitoneal inoculation of Salmonella choleraesuis 31N-1 using an enzyme-linked immunosorbent assay and flow cytometry. Results: TLR2 gene was abundantly expressed by NKT cells freshly isolated from naive mice. FasL expression on liver NKT cells increased in TLR2(-/-) mice but not in TLR2(-/-) mice after Salmonella infection. Serum alanine aminotransferase level was significantly lower in the TLR2(-/-) and gld/gld mice than in the control mice after infection. Conclusions: TLR2 may contribute to liver injury induced by Salmonella infection via FasL induction on liver NKT cells.
引用
收藏
页码:1265 / 1277
页数:13
相关论文
共 64 条
[1]   CYTOTOXICITY OF FRESH NK1.1(+) T-CELL RECEPTOR ALPHA/BETA(+) THYMOCYTES AGAINST A CD4+8+ THYMOCYTE POPULATION ASSOCIATED WITH INTACT FAS ANTIGEN EXPRESSION ON THE TARGET [J].
ARASE, H ;
ARASE, N ;
KOBAYASHI, Y ;
NISHIMURA, Y ;
YONEHARA, S ;
ONOE, K .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (02) :423-432
[2]   Role of reactive oxygen intermediates in activation-induced CD95 (APO-1/Fas) ligand expression [J].
Bauer, MKA ;
Vogt, M ;
Los, M ;
Siegel, J ;
Wessellborg, S ;
Schulze-Osthoff, K .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (14) :8048-8055
[3]   A conserved signaling pathway: The Drosophila Toll-Dorsal pathway [J].
Belvin, MP ;
Anderson, KV .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1996, 12 :393-416
[4]   Mouse CD1-specific NK1 T cells: Development, specificity, and function [J].
Bendelac, A ;
Rivera, MN ;
Park, SH ;
Roark, JH .
ANNUAL REVIEW OF IMMUNOLOGY, 1997, 15 :535-562
[5]   CD1d-mediated recognition of an α-galactosylceramide by natural killer T cells is highly conserved through mammalian evolution [J].
Brossay, L ;
Chioda, M ;
Burdin, N ;
Koezuka, Y ;
Casorati, G ;
Dellabona, P ;
Kronenberg, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (08) :1521-1528
[6]  
Brossay L, 1998, J IMMUNOL, V161, P5124
[7]  
Burdin N, 1998, J IMMUNOL, V161, P3271
[8]   Requirement for V(alpha)14 NKT cells in IL-12-mediated rejection of tumors [J].
Cui, JQ ;
Shin, T ;
Kawano, T ;
Sato, H ;
Kondo, E ;
Toura, I ;
Kaneko, Y ;
Koseki, H ;
Kanno, M ;
Taniguchi, M .
SCIENCE, 1997, 278 (5343) :1623-1626
[9]  
ElNewihi HM, 1996, HEPATOLOGY, V24, P516, DOI 10.1053/jhep.1996.v24.pm0008781316
[10]   PLASMA TUMOR NECROSIS FACTOR-ALPHA PREDICTS DECREASED LONG-TERM SURVIVAL IN SEVERE ALCOHOLIC HEPATITIS [J].
FELVER, ME ;
MEZEY, E ;
MCGUIRE, M ;
MITCHELL, MC ;
HERLONG, HF ;
VEECH, GA ;
VEECH, RL .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1990, 14 (02) :255-259