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Expression of Suppressors of Cytokine Signaling-3 in Helicobacter pylori-Infected Rat Gastric Mucosal RGM-1 Cells

机译:细胞因子信号传导抑制剂3在幽门螺杆菌感染的大鼠胃粘膜RGM-1细胞中的表达

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Our previous studies show that Helicobacter pylori (H. pylori) induces oxidative stress and the expression of proinflamma tory cytokines in gastric epithelial cells. H. pylori induces the expression of molecular chaperones and proteins involved in protein-folding ma chinery as a defense mechanism against cellular stress. The suppressors of cytokine signaling (SOCS) are known as negative regulators of ma jor immune signal pathways. The purpose of this article is to determine whether H. pylori in a Korean isolate (HP99) induces the expression of SOCS in rat gastric mucosal RGM-1 cells as a defense mechanism. As a result, HP99 induced SOCS-3 expression time-dependently in RGM-1 cells. SOCS-1 was not expressed while SOCS-2 expression was not changed by HP99 infection in RGM-1 cells. SOCS-3 might have a de fensive role in H. pylori-infected gastric mucosal cells. Further study by manipulating SOCS-3 gene should be performed to investigate the phys iological meaning of SOCS-3 induced by H. pylori in gastric mucosal cells.
机译:我们以前的研究表明,幽门螺杆菌(H. pylori)在胃上皮细胞中诱导氧化应激和前炎症细胞因子的表达。幽门螺杆菌诱导参与蛋白质折叠机械的分子伴侣和蛋白质的表达,作为抵抗细胞应激的防御机制。细胞因子信号传导(SOCS)的抑制剂被称为主要免疫信号通路的负调节剂。本文的目的是确定韩国分离株(HP99)中的幽门螺杆菌是否诱导大鼠胃粘膜RGM-1细胞中SOCS的表达,作为防御机制。结果,HP99在RGM-1细胞中诱导了SOCS-3表达的时间依赖性。在RGM-1细胞中,HP99感染不会使SOCS-1表达,而不会使SOCS-2表达改变。 SOCS-3可能在幽门螺杆菌感染的胃粘膜细胞中具有防御作用。应通过操纵SOCS-3基因进行进一步研究,以研究幽门螺杆菌在胃粘膜细胞中诱导SOCS-3的生理学意义。

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