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首页> 外文期刊>World Journal of Gastroenterology >H pylori receptor MHC class Ⅱ contributes to the dynamic gastric epithelial apoptotic response
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H pylori receptor MHC class Ⅱ contributes to the dynamic gastric epithelial apoptotic response

机译：H幽门螺杆菌受体MHCⅡ类参与动态胃上皮细胞凋亡反应

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AIM: To investigate the role of MHC class Ⅱ in the modulation of gastric epithelial cell apoptosis induced by H pylori infection. METHODS: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC class Ⅱ and CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively. RESULTS: Pretreatment of N87 cells with the anti-MHC class Ⅱ IgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection. When caspase 3 activation was specifically measured, crosslinking of MHC class Ⅱ resulted in markedly reduced caspase activation, while simple ligation of MHC class Ⅱ did not. Crosslinking of MHC class Ⅱ also resulted in an increased activation of the anti-apoptosis molecule BCL-2 compared to simple ligation. Confocal microscope analysis demonstrated that the pretreatment of gastric epithelial cells with a crosslinking anti-MHC class Ⅱ IgM blocked the recruitment of FADD to the cell surface. CONCLUSION: The ability of MHC class Ⅱ to modulate gastric epithelial apoptosis is at least partially dependent on its crosslinking. The crosslinking of this molecule has anti-apoptotic effects during the earlier time points of H pylori infection. This effect is possibly mediated by the ability of MHC class Ⅱ to modulate the activation of the pro-apoptotic receptor Fas by blocking the recruitment of the accessory molecule FADD, and this delay in apoptosis induction could allow for prolonged cytokine secretion by H pylori-infected gastric epithelial cells.
机译：目的：探讨Ⅱ类MHC在幽门螺杆菌感染诱导的胃上皮细胞凋亡调控中的作用。方法：用特异于MHCⅡ类和CD95的细菌或激动剂抗体刺激人胃上皮细胞系后，对细胞凋亡和抗凋亡事件进行定量，包括半胱天冬酶激活，BCL-2激活和FADD募集。荧光测定，细胞计数珠阵列和共聚焦显微镜。结果：用抗MHCⅡ类IgM抗体RFD1预处理N87细胞可降低幽门螺杆菌感染后24 h的整体胱天蛋白酶活化。当专门测量caspase 3激活时，MHCⅡ类的交联导致caspase激活显着降低，而MHCⅡ类的简单连接却没有。与简单的连接相比，MHCⅡ类的交联还导致抗凋亡分子BCL-2的活化增加。共聚焦显微镜分析表明，用交联抗MHCⅡ类IgM预处理胃上皮细胞可阻止FADD募集到细胞表面。结论：MHCⅡ类调节胃上皮细胞凋亡的能力至少部分取决于其交联。该分子的交联在幽门螺杆菌感染的较早时间点具有抗凋亡作用。这种作用可能是由MHCⅡ类通过阻止辅助分子FADD的募集来调节促凋亡受体Fas激活的能力所介导的，这种细胞凋亡诱导的延迟可能使幽门螺杆菌感染的细胞因子分泌延长。胃上皮细胞。

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