M Nakao1, P Malfertheiner. 1. Pharmaceutical Research Laboratories III, Takeda Chemical Industries Ltd., Osaka, Japan.
Abstract
BACKGROUND: Helicobacter pylori plays a role in the pathogenesis of both duodenal and gastric ulcers. The aim of this study was to evaluate the effect of the proton pump inhibitor (PPI), lansoprazole, commonly used in eradication regimens, on growth, bactericidal activity and morphology of H. pylori in vitro in comparison with other PPIs. MATERIALS AND METHODS: Growth inhibitory activity of each of the PPIs was evaluated by determining minimum inhibitory concentrations using an agar dilution method. Bactericidal activity was determined by analysis of the viable cells in culture at various time points after incubation with different concentrations of the PPIs. Bacterial morphology was examined using scanning electron microscopy of fixed cells after exposure to the test substances. Urease activity in cell extracts of H. pylori that had been incubated with increasing concentrations of the PPIs was determined by colorimetry. RESULTS: The growth inhibitory activity of lansoprazole was significantly more potent than that of omeprazole or pantoprazole (MIC90 6.25 vs. 25 and 100 micrograms/ml, respectively). Exposure of H. pylori to lansoprazole produced loss of viability and an aberrant bacterial morphology, which was more extensive than seen with omeprazole or pantoprazole. Lansoprazole dose dependently inhibited urease activity; its effectiveness was comparable with omeprazole but more potent than pantoprazole. CONCLUSIONS: The mechanism of action that leads to loss of viability of H. pylori cells appears to differ between the three PPIs investigated; lansoprazole was the most potent of the three agents in terms of growth inhibition and disruption of bacterial morphology.
BACKGROUND:Helicobacter pylori plays a role in the pathogenesis of both duodenal and gastric ulcers. The aim of this study was to evaluate the effect of the proton pump inhibitor (PPI), lansoprazole, commonly used in eradication regimens, on growth, bactericidal activity and morphology of H. pylori in vitro in comparison with other PPIs. MATERIALS AND METHODS: Growth inhibitory activity of each of the PPIs was evaluated by determining minimum inhibitory concentrations using an agar dilution method. Bactericidal activity was determined by analysis of the viable cells in culture at various time points after incubation with different concentrations of the PPIs. Bacterial morphology was examined using scanning electron microscopy of fixed cells after exposure to the test substances. Urease activity in cell extracts of H. pylori that had been incubated with increasing concentrations of the PPIs was determined by colorimetry. RESULTS: The growth inhibitory activity of lansoprazole was significantly more potent than that of omeprazole or pantoprazole (MIC90 6.25 vs. 25 and 100 micrograms/ml, respectively). Exposure of H. pylori to lansoprazole produced loss of viability and an aberrant bacterial morphology, which was more extensive than seen with omeprazole or pantoprazole. Lansoprazole dose dependently inhibited urease activity; its effectiveness was comparable with omeprazole but more potent than pantoprazole. CONCLUSIONS: The mechanism of action that leads to loss of viability of H. pylori cells appears to differ between the three PPIs investigated; lansoprazole was the most potent of the three agents in terms of growth inhibition and disruption of bacterial morphology.
Authors: Laura Cerqueira; Ricardo M Fernandes; Rui M Ferreira; Mónica Oleastro; Fátima Carneiro; Catarina Brandão; Pedro Pimentel-Nunes; Mário Dinis-Ribeiro; Céu Figueiredo; Charles W Keevil; Maria J Vieira; Nuno F Azevedo Journal: J Clin Microbiol Date: 2013-04-17 Impact factor: 5.948