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

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 microg/mL versus control, 1,853 +/- 262 microg/mL; < 0.05). Plasma CINC levels were significantly increased after 6 hours in the cerulein hyperstimulation model (1,680 +/- 134 microg/mL versus control, 725 +/- 128 microg/mL; < 0.005) and after 3 hours in the bile salt infusion model (6,663 +/- 1,405 microg/mL versus control, 2,339 +/- 800 microg/mL; < 0.05).

CONCLUSION

CINC and MCP-1/JE may be early mediators of the inflammatory response in acute pancreatitis.