INTERACTION OF HELICOBACTER-PYLORI AND ITS FATTY-ACIDS WITH PARIETAL-CELLS AND GASTRIC H+/K+-ATPASE

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+/R(+)-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 Hi 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 9,10-methyleneoctadecanoic acid tetradecanoic acid are probably the acid inhibitory factors secreted by H pylori.