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

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PANCREAS
卷 25, 期 3, 页码 260-269

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00006676-200210000-00008

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acute pancreatitis; cerulein; chemokines; CINC-1; MCP-1/JE

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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.

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