Expression of the chemokines MCP-1/JE and cytokine-induced neutrophil chemoattractant in early acute pancreatitis
Expression of the chemokines MCP-1/JE and cytokine-induced neutrophil chemoattractant in early acute pancreatitis
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DOI：
10.1097/00006676-200210000-00008
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发表时间：
2002-10-01
期刊：
影响因子：
2.9
通讯作者：
Slavin, J
中科院分区：
文献类型：
--
作者：
Brady, M;Bhatia, M;Slavin, J
简介：炎症介质在急性胰腺炎中起着至关重要的作用。趋化因子家族成员所发挥的确切作用仍不清楚。目的：探讨早期急性胰腺炎中CC趋化因子单核细胞趋化蛋白（MCP）-1/JE和CXC趋化因子细胞因子诱导的中性粒细胞趋化蛋白（CINC）的表达。方法：通过腹腔注射雨蛙素或向胰管内输注 5% 牛磺胆酸钠来诱发大鼠胰腺炎。通过免疫组织化学、酶联免疫吸附测定 (ELISA)、Northern 分析和定量实时逆转录酶聚合酶链反应 (RT-PCR) 测定胰腺和血浆中 MCP-1/JE 和 CINC 的表达。结果：诱发急性胰腺炎后，在腺泡细胞中观察到 MCP-1/JE 和 CINC 免疫反应性。浸润性中性粒细胞被抗 MCP-1/JE 抗体强烈免疫标记，而巨噬细胞与 CINC 抗体强烈反应。 Northern 分析和定量实时 RT-PCR 证明胰腺组织中 MCP-1/JE 和 CINC mRNA 水平上调。在雨蛙蛋白过度刺激模型中 6 小时后，血浆 MCP-1 水平显着增加（2,444 +/- 93 微克/毫升，对照为 1,853 +/- 262 微克/毫升；p < 0.05）。在雨蛙蛋白过度刺激模型中，血浆 CINC 水平在 6 小时后显着升高（与对照相比，1,680 +/- 134 微克/毫升，725 +/- 128 p < 0.005），在胆汁盐输注模型中 3 小时后（与对照相比，6,663 +/- 1,405 微克/毫升，2,339 +/- 800 微克/毫升；p < 0.005），血浆 CINC 水平显着升高。 0.05）。结论：CINC和NICP-1/JE可能是急性胰腺炎炎症反应的早期介质。
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.