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大鼠胰蛋白酶诱导的急性胰腺炎中胰腺的早期细菌感染及病程

Early bacterial infection of the pancreas and course of disease in cerulein-induced acute pancreatitis in rats.

作者信息

Manes G, Kahl S, Schulz H-U, Lippert H, Ferrara E C, Malfertheiner P

机构信息

Department of Gastroenterology, Otto von Guericke University Magdeburg, Germany.

出版信息

Dig Liver Dis. 2006 Jun;38(6):423-8. doi: 10.1016/j.dld.2006.02.019. Epub 2006 Apr 14.

Abstract

BACKGROUND

Bacterial infection of the pancreas aggravates the course of acute pancreatitis. Since bacterial translocation from the gut is likely to be an early event, in an animal model of pancreatitis, we investigated the effect of early bacterial supra-infection of the pancreas on the course of the disease.

METHODS

Six hours after the induction of acute pancreatitis in male Wistar rats (n = 180) by supramaximal stimulation with cerulein (or placebo in a control group), the animals were operated and a suspension of Helicobacter pylori, Escherichia coli or saline were introduced either in the pancreatic duct or interstitium (12 groups of 15 rats each); after 24 h, animals were killed and the following parameters analysed: macroscopic and histologic appearance of the pancreas (score), wet-to-dry weight ratio, pancreas trypsinogen activation peptide level, serum amylase, interleukin-6 and phospholipase A2 activity.

RESULTS

All parameters were increased in rats with cerulein-induced pancreatitis in comparison to placebo. Interstitial and intraductal application of bacteria increased the pancreatic damage. This effect was more evident with the application of E. coli in both cerulein and placebo groups. Application of E. coli but not of H. pylori determined pancreatic activation of trypsinogen, increased mortality and induced the production of interleukin-6.

CONCLUSIONS

Bacterial invasion of the pancreas worsens the histologic and clinical picture of disease and induces a systemic inflammatory response.

摘要

背景

胰腺细菌感染会加重急性胰腺炎的病程。由于肠道细菌移位很可能是早期事件,在胰腺炎动物模型中,我们研究了胰腺早期细菌超感染对疾病病程的影响。

方法

用雨蛙肽超最大刺激诱导雄性Wistar大鼠(n = 180)发生急性胰腺炎6小时后(对照组注射安慰剂),对动物进行手术,将幽门螺杆菌、大肠杆菌悬液或生理盐水注入胰管或胰腺间质(共12组,每组15只大鼠);24小时后,处死动物并分析以下参数:胰腺的大体和组织学表现(评分)、湿重与干重比、胰腺胰蛋白酶原激活肽水平、血清淀粉酶、白细胞介素-6和磷脂酶A2活性。

结果

与安慰剂组相比,雨蛙肽诱导的胰腺炎大鼠所有参数均升高。细菌的间质内和导管内注入增加了胰腺损伤。在雨蛙肽组和安慰剂组中,注入大肠杆菌时这种效应更明显。注入大肠杆菌而非幽门螺杆菌可导致胰蛋白酶原的胰腺激活、死亡率增加并诱导白细胞介素-6的产生。

结论

胰腺细菌入侵会使疾病的组织学和临床表现恶化,并引发全身炎症反应。

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