Expression of the chemokines MCP-1/JE and cytokine-induced neutrophil chemoattractant in early acute pancreatitis

被引:51
作者
Brady, M
Bhatia, M
Christmas, S
Boyd, MT
Neoptolemos, JP
Slavin, J
机构
[1] Univ Liverpool, Royal Liverpool Univ Hosp, Dept Surg, Liverpool L69 3GA, Merseyside, England
[2] Univ Liverpool, Dept Immunol, Liverpool L69 3GA, Merseyside, England
关键词
acute pancreatitis; cerulein; chemokines; CINC-1; MCP-1/JE;
D O I
10.1097/00006676-200210000-00008
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Introduction: Inflammatory mediators play a critical role in acute pancreatitis. The precise role played by members of the chemokine family remains unclear. Aims: To investigate the expression of the CC chemokine monocyte chemotactic protein (MCP)-1/JE and the CXC chemokine cytokine-induced neutrophil chemoattractant (CINC) in early acute pancreatitis. Methodology: Pancreatitis was induced in rats, either by intraperitoneal injection of cerulein or by infusion of 5% sodium taurocholate into the pancreatic duct. Expression of MCP-1/JE and CINC in pancreas and plasma was determined by immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), Northern analysis, and quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR). Results: Following induction of acute pancreatitis, MCP-1/JE and CINC immunoreactivity was seen in acinar cells. Infiltrating neutrophils Were strongly immunolabeled with an anti-MCP-1/JE antibody, whereas macrophages reacted strongly with an antibody to CINC. Northern analysis and quantitative real-time RT-PCR demonstrated upregulation of MCP-1/JE and CINC mRNA levels in pancreatic tissue. Plasma MCP-1 levels were significantly increased after 6 hours in the cerulein hyperstimulation model (2,444 +/- 93 mug/mL versus control, 1,853 +/- 262 mug/mL; p < 0.05). Plasma CINC levels were significantly increased after 6 hours in die cerulein hyperstimulation model ( 1,680 +/- 134 mug/ml versus control, 725 +/- 128 p < 0.005) and after 3 hours in the bile salt infusion model (6,663 +/- 1,405 mug/mL versus control, 2,339 +/- 800 mug/mL; p < 0.05). Conclusion: CINC and NICP-1/JE may be early mediators of the inflammatory response in acute pancreatitis.
引用
收藏
页码:260 / 269
页数:10
相关论文
共 40 条
[1]   Chemokines: Leucocyte recruitment and activation cytokines [J].
Adams, DH ;
Lloyd, AR .
LANCET, 1997, 349 (9050) :490-495
[2]   Role of CD18-ICAM-1 in the entrapment of stimulated leukocytes in alveolar capillaries of perfused rat lungs [J].
Aoki, T ;
Suzuki, Y ;
Nishio, K ;
Suzuki, K ;
Miyata, A ;
Iigou, Y ;
Serizawa, H ;
Tsumura, H ;
Ishimura, Y ;
Suematsu, M ;
Yamaguchi, K .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 273 (05) :H2361-H2371
[3]   Changes in polyamine content, arginine and ornithine decarboxylases and transglutaminase activities during light/dark phases (of initial differentiation) in maize calluses and their chloroplasts [J].
Bernet, E ;
Claparols, I ;
Dondini, L ;
Santos, MA ;
Serafini-Fracassini, D ;
Torné, JM .
PLANT PHYSIOLOGY AND BIOCHEMISTRY, 1999, 37 (12) :899-909
[4]  
Bhatia M, 1998, INT J PANCREATOL, V24, P77
[5]   Treatment with neutralising antibody against cytokine induced neutrophil chemoattractant (CINC) protects rats against acute pancreatitis associated lung injury [J].
Bhatia, M ;
Brady, M ;
Zagorski, J ;
Christmas, SE ;
Campbell, F ;
Neoptolemos, JP ;
Slavin, J .
GUT, 2000, 47 (06) :838-844
[6]  
BHATIA M, 1999, PANCREAS, V19, P415
[7]   Role of CC chemokines (macrophage inflammatory protein-1β, monocyte chemoattractant protein-1, RANTES) in acute lung injury in rats [J].
Bless, NM ;
Huber-Lang, M ;
Guo, RF ;
Warner, RL ;
Schmal, H ;
Czermak, BJ ;
Shanley, TP ;
Crouch, LD ;
Lentsch, AB ;
Sarma, V ;
Mulligan, MS ;
Friedl, HP ;
Ward, PA .
JOURNAL OF IMMUNOLOGY, 2000, 164 (05) :2650-2659
[8]   PLASMA-LEVELS OF THE CHEMOKINES MONOCYTE CHEMOTACTIC PROTEIN-1 AND PROTEIN-2 ARE ELEVATED IN HUMAN SEPSIS [J].
BOSSINK, AWJ ;
PAEMEN, L ;
JANSEN, PM ;
HACK, CE ;
THIJS, LG ;
VANDAMME, J .
BLOOD, 1995, 86 (10) :3841-3847
[9]   Multiple chemotactic factors: fine control or redundancy? [J].
Devalaraja, MN ;
Richmond, A .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1999, 20 (04) :151-156
[10]  
Fan J, 1998, J IMMUNOL, V161, P440