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巴弗洛霉素A1抑制幽门螺杆菌诱导的HeLa细胞空泡化。

Bafilomycin A1 inhibits Helicobacter pylori-induced vacuolization of HeLa cells.

作者信息

Papini E, Bugnoli M, De Bernard M, Figura N, Rappuoli R, Montecucco C

机构信息

Dipartimento di Scienze Biomediche, Università di Padova, Italy.

出版信息

Mol Microbiol. 1993 Jan;7(2):323-7. doi: 10.1111/j.1365-2958.1993.tb01123.x.

Abstract

Bafilomycin A1, a specific inhibitor of the vacuolar-type H(+)-ATPase, responsible for acidification of intracellular compartments, prevents the vacuolization of Hela cells induced by H. pylori, with an inhibitory concentration giving 50% of maximal (ID50) of 4 nM. Bafilomycin A1 is also very efficient in restoring vacuolated cells to a normal appearance. The vacuolating activity of Helicobacter pylori is not inhibited by a series of specific inhibitors of vacuolar H(+)-ATPases. These findings indicate that a transmembrane pH gradient is needed for the formation and growth of vacuoles caused by the bacterium and that this pH gradient is due to the activity of a vacuolar ATPase proton pump of HeLa cells.

摘要

巴弗洛霉素A1是液泡型H(+) -ATP酶的特异性抑制剂,负责细胞内区室的酸化,它可防止幽门螺杆菌诱导的HeLa细胞空泡化,其半数抑制浓度(ID50)为4 nM。巴弗洛霉素A1在使空泡化细胞恢复正常外观方面也非常有效。一系列液泡型H(+) -ATP酶的特异性抑制剂均不能抑制幽门螺杆菌的空泡化活性。这些发现表明,细菌引起的空泡形成和生长需要跨膜pH梯度,并且这种pH梯度是由于HeLa细胞液泡ATP酶质子泵的活性所致。

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