首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Helicobacter infection and phospholipase A_2 enzymes: Effect of Helicobacter felis-infection on the expression and activity of sPLA_2 enzymes in mouse stomach
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Helicobacter infection and phospholipase A_2 enzymes: Effect of Helicobacter felis-infection on the expression and activity of sPLA_2 enzymes in mouse stomach

机译:幽门螺杆菌感染和磷脂酶A_2酶:幽门螺杆菌感染对小鼠胃中sPLA_2酶表达和活性的影响

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摘要

The murine gastric mucosa possesses very high secretory type phospholipase A_2 activity. Northern and Western blots indicated that the pancreatic-type, sPLA_2-IB represents the predominant form of sPLA_2 enzymes present in the gastric mucosa. Both sPLA_2-IB mRNA and protein in the gastric mucosa exceeded levels found in the pancreas, and in contrast to the pancreatic enzyme it was present primarily in the active state. The sPLA_2-IB gene is not expressed in the murine small intestine and colon. Infection by the gastritis-inducing bacteria, Helicobacter felis (H. felis) dramatically and time dependently decreased the PLA_2 activity in the glandular stomach of the mouse strain, C57BL/6, sensitive to the organism, which appeared to be related to a decrease in the percentage of sPLA_2-IB present in the active form. This bacterial-induced reduction in PLA_2 activity was not observed in BALB/c mice that fail to develop gastritis in response to H. felis infection. C57BL/6 mice do not, while BALB/c mice express, the PLA_2-II enzyme. The H. felis-induced reduction in sPLA_2-IB activity may weaken the gastric barrier by reducing the local concentration of arachidonic and linoleic acid, liberated from membrane phospholipids, the major precursors of 'cytoprotective' prostaglandins. Data presented here suggest that both sPLA_2-IB and sPLA_2-II enzymes may contribute to the gastric response to Helicobacter infection.
机译:鼠胃粘膜具有很高的分泌型磷脂酶A_2活性。 Northern和Western印迹表明,胰腺类型的sPLA_2-IB代表胃粘膜中sPLA_2酶的主要形式。胃粘膜中的sPLA_2-IB mRNA和蛋白质均超过了胰腺中的水平,与胰腺酶相反,它主要以活性状态存在。 sPLA_2-IB基因不在鼠小肠和结肠中表达。引起胃炎的细菌感染幽门螺杆菌(H. felis)显着且时间依赖性地降低了对这种生物体敏感的小鼠品系C57BL / 6的腺胃中PLA_2的活性,这似乎与细菌的减少有关。活性形式中sPLA_2-IB的百分比。在BALB / c小鼠中未观察到这种细菌诱导的PLA_2活性降低,而BALB / c小鼠未能响应H. felis感染而发展为胃炎。 C57BL / 6小鼠不表达,而BALB / c小鼠表达PLA_2-II酶。 H. felis诱导的sPLA_2-IB活性降低可能会通过降低从膜磷脂(“细胞保护性”前列腺素的主要前体)释放的花生四烯酸和亚油酸的局部浓度来削弱胃屏障。此处提供的数据表明,sPLA_2-IB和sPLA_2-II酶都可能对胃对幽门螺杆菌感染的反应有所贡献。

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