IL-22诱导胃上皮细胞释放炎症因子并促进淋巴细胞趋化

IL-22 induces gastric epithelial cell to produce inflammatory factors which promote lymphocyte chemotaxis

为探讨IL-22在胃部炎症中的作用,我们采用流式细胞术和组织免疫荧光染色检测胃上皮细胞系AGS细胞及胃组织中IL-22受体的表达;采用IL22刺激胃上皮细胞系AGS及GES-1细胞,定量PCR检测其S100钙结合蛋白(S100)A8、S100A9、IL-8、基质金属蛋白酶(MMP)-1、MMP-10的表达;通过Transwell细胞趋化试验检测IL-22对淋巴细胞的趋化作用。结果发现,胃上皮细胞系及胃组织中有IL-22R1表达,并且IL-22能够诱导胃上皮细胞产生炎症因子及MMP,某些因子可促进淋巴细胞趋化。据此说明IL-22通过调控胃上皮细胞产生炎症因子并趋化淋巴细胞浸润,参与胃部炎症反应。

To investigate the role of IL22 in gastric inflammation, gastric epithelial cell line AGS and gastric tissue were col lected to detect IL22 receptor expression by flow cytometry and immunofluorescence staining. Gastric epithelial cell lines AGS and GES1 were stimulated with IL22 and cells were collected for analysis of expression of $100A8, S100Ag, IL8, MMP1 and MMP10 mRNA by realtime PCR. The influence of IL22 on lymphocyte chemotaxis was detected by Transwell chemotax is assay. The results showed that IL22R1 expression was positive in the two gastric epithelial cell lines and gastric tissue, and IL22 significantly induced inflammatory factors and MMPs mRNA expression in gastric epithelial cell lines. Transwell chemo taxis assay showed that IL22 could induce much more lymphocytes in the lower chamber than does AGS cells alone. Taken to gether, these results suggest that 1L 22 participate in inflammatory reaction by regulating inflammatory factors expressions and inducing inflammatory cell infiltration.