摘要
目的探讨急性胆道感染时大鼠肝组织中脂多糖(lipopolysaccharide,LPS)受体CD14的表达及其对细胞因子分泌的影响。方法通过结扎Wistar大鼠胆总管,在胆总管内注入大肠杆菌O111∶B4,复制急性胆道感染动物模型。于术后0、3、6、12、24 h分别检测肝组织中CD14蛋白和mRNA表达水平,血浆内毒素、TNF-α和IL-6的含量、枯否细胞(kupffer cells,KCs)吞噬活性,电镜观察KCs超微结构的变化。结果在急性胆道感染时随着感染时间延长,血浆内毒素浓度逐渐升高,KCs呈现激活的改变,血浆TNF-α、IL-6含量明显增加,而此时肝组织中CD14的表达也显著增加。结论急性胆道感染时肝组织中CD14的表达进行性增强,KCs激活,释放的细胞因子也逐渐增多,这可能是急性胆道感染时KCs致炎作用增强的重要机制之一。
Objective To study the expression of lipopolysaccharide （LPS） receptor, CD14 in the liver tissue during acute biliary infection and its relation with production of cytokines. Methods Rat models of acute biliary infection were established by ligating the choledochus and injecting Escherichia coli O111：B4 into the duct. The expressions of CD14 protein and mRNA in liver tissue, the plasma levels of endotoxin, TNF-α and IL-6, and phagocytosis activity of Kupffer cells （KCs） were assayed at 0, 3, 6, 12 and 24 h after operation. Ultrastructural changes in KCs were observed by electron microscopy. Results With the course prolonging in acute biliary infection, the plasma endotoxin level was progressively increased, KCs were activated and the levels of TNF-α and IL-6 markedly were increased, while the CD14 expression obviously increased at mRNA and protein levels. Conclusion The CD14 expression is gradually increased in liver tissue during acute biliary infection. KCs are activated and releasing more and more cytokines. It might be one of the important mechanisms of that KCs improve inflammatory response during the infection.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2009年第8期672-674,共3页
Journal of Third Military Medical University
基金
国家自然科学基金(30500473)~~
