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. 1994 Sep;35(9):1176–1180. doi: 10.1136/gut.35.9.1176

Interaction of Helicobacter pylori and its fatty acids with parietal cells and gastric H+/K(+)-ATPase.

W Beil 1, C Birkholz 1, S Wagner 1, K F Sewing 1
PMCID: PMC1375690  PMID: 7959221

Abstract

Helicobacter pylori and the fatty acids produced by this organism were compared for their acid inhibitory activity in isolated parietal cells and their interaction with gastric H+/K(+)-ATPase. H pylori (intact organisms, sonicates, methanolic extracts, and extracts from culture medium) and the fatty acids cis 9,10-methyleneoctadecanoic acid and tetradecanoic acid inhibited at fairly high concentrations histamine- and dibutyryl cyclic adenosine monophosphate stimulated acid production in isolated parietal cells, dissipated (with a slow onset) the H+/K(+)-ATPase created H+ gradient in gastric membrane vesicles, and inhibited H+/K(+)-ATPase activity in a concentration dependent manner. The inhibitory potency of H pylori and the fatty acids in relation to H+/K(+)-ATPase depended on the amount of membrane protein. Bovine serum albumin prevented enzyme inhibition and proton dissipation from gastric vesicles. The data indicate that H pylori establishes its antisecretory action in parietal cells by blocking H+/K(+)-ATPase activity and also by a detergent action at the apical parietal cell membrane. The fatty acids cis 9,10-methyleneoctadecanoic acid and tetradecanoic acid are probably the acid inhibitory factors secreted by H pylori.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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