大肠埃希菌诱导小肠上皮细胞产生β防御素-3的机制

Mechanism of induction of β-defensin 3 production in intestinal epithelial cells by E.coli

目的探讨大肠埃希菌诱导小肠上皮细胞产生β防御素-3(mouseβ-defensin 3,mBD-3)的机制。方法用大肠埃希菌作用于小肠上皮细胞0、24和48 h后,MTT法检测细胞增殖情况;免疫组化荧光法检测mBD-3的表达;Western blot法检测丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)通路中p-ERK1/2、p-JNK及p-p38的表达。结果大肠埃希菌作用小肠上皮细胞48 h时,细胞生长率最低,为(7. 12±0. 31)%;mBD-3的表达在48 h时最高;p-ERK1/2的表达在48 h时最高,显著高于0和24 h(P <0. 01)。结论大肠埃希菌抑制小肠上皮细胞的增殖,并促进mBD-3的表达,这种促进机制是通过ERK1/2途径实现。

Objective To investigate the mechanism of E. coli in induction of mouse β-defensin 3（mBD-3） production in intestinal epithelial cells. Methods Intestinal epithelial cells were treated with E. coli for 0,24 and 48 h and determined for proliferation by MTT assay. The expression of mBD-3 was determined by immunocytochemistry,while those of p-ERK1/2,p-JNK and p-p38 in MAPK pathway by Western blot. Results The growth rate of intestinal epithelial cells after treatment with E. coli for 48 h was the lowest,which was（7. 12 ± 0. 31）%. Both the expression levels of mBD-3 and p-ERK1/2 reached the maximum after treatment for 48 h. The expression level of p-ERK1/2 48 h was significantly higher than those 0 and 24 h after treatment（P〈0. 01）. Conclusion E. coli inhibited the proliferation of intestinal epithelial cells,and promoted the expression of mBD-3 by ERK1/2 pathway.