Maekawa T, Kinoshita Y, Matsushima Y, Okada A, Fukui H, Waki S, Kishi K, Kawanami C, Nakata H, Hassan S, Wakatsuki Y, Ota H, Amano K, Nakao M, Chiba T
Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Japan.
J Lab Clin Med. 1997 Oct;130(4):442-9. doi: 10.1016/s0022-2143(97)90045-7.
Although Helicobacter pylori has been reported to stimulate the release of various cytokines from gastric tissue, it remains unknown whether normal and nontumorous gastric epithelial cells produce these cytokines. Therefore, in this study, we used a normal mouse gastric surface mucous cell line (GSM06) to determine whether gastric epithelial cells produce proinflammatory cytokines in response to H. pylori. The expression of MHC class II antigen was also examined, to investigate whether gastric epithelial cells participate in the immune response to H. pylori. In the study, GSM06 cells were incubated with H. pylori or its lipopolysaccharide (LPS). Proinflammatory cytokines were detected by Northern and Western blot analysis. The expression of MHC class II antigen was examined by fluorescence activated cell sorter (FACS) analysis. Genetic expression of proinflammatory cytokines such as interleukin-1alpha, tumor necrosis factor-alpha, and cytokine-induced neutrophil chemoattractant-2beta was enhanced by both intact and sonicated H. pylori, but not by H. pylori LPS. The expression of MHC class II antigen was induced by H. pylori more strongly than by interferon-gamma. We conclude that H. pylori induces the expression of proinflammatory cytokines and MHC class II antigen in gastric epithelial cells. Gastric epithelial cells may act as antigen-presenting cells and participate in the immune response to H. pylori infection.
虽然已有报道称幽门螺杆菌可刺激胃组织释放多种细胞因子,但正常和非肿瘤性胃上皮细胞是否产生这些细胞因子仍不清楚。因此,在本研究中,我们使用正常小鼠胃表面黏液细胞系(GSM06)来确定胃上皮细胞是否会因幽门螺杆菌而产生促炎细胞因子。我们还检测了MHC II类抗原的表达,以研究胃上皮细胞是否参与对幽门螺杆菌的免疫反应。在该研究中,将GSM06细胞与幽门螺杆菌或其脂多糖(LPS)一起孵育。通过Northern和Western印迹分析检测促炎细胞因子。通过荧光激活细胞分选仪(FACS)分析检测MHC II类抗原的表达。完整的和超声处理的幽门螺杆菌均可增强白细胞介素-1α、肿瘤坏死因子-α和细胞因子诱导的中性粒细胞趋化因子-2β等促炎细胞因子的基因表达,但幽门螺杆菌LPS则无此作用。幽门螺杆菌诱导MHC II类抗原表达的作用比干扰素-γ更强。我们得出结论,幽门螺杆菌可诱导胃上皮细胞中促炎细胞因子和MHC II类抗原的表达。胃上皮细胞可能作为抗原呈递细胞参与对幽门螺杆菌感染的免疫反应。