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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。
In order to investigate the role of IL-22 in gastric inflammation, we used flow cytometry and tissue immunofluorescence staining to detect the expression of IL-22 receptor in gastric epithelial cell line AGS and gastric tissue. IL22 stimulated gastric epithelial cell line AGS and GES-1 cells. The expression of S100, S100A9, IL-8, MMP-1 and MMP-10 in S100 calcium-binding protein was detected by quantitative polymerase chain reaction 22 Chemotaxis to lymphocytes. The results showed that gastric epithelial cells and gastric tissue IL-22R1 expression, and IL-22 can induce gastric epithelial cells produce inflammatory cytokines and MMP, some of the factors can promote lymphocyte chemotaxis. This shows that IL-22 through the regulation of gastric epithelial cells produce inflammatory cytokines and chemotactic lymphocyte infiltration, involved in gastric inflammation.