BACKGROUND/AIMS: Helicobacter felis colonizes the gastric mucosa of rodents. Preliminary studies showed differences in the distribution of the organism in different parts of the stomach that seemed related to the secretory capacity of the mucosa. The aim of this study was to determine the localization of H. felis in the mouse stomach and to investigate the influence of acid-suppressive agents. METHODS: Specific-pathogen-free BALB/c mice were infected with H. felis. Colonization was assessed in longitudinal sections of gastric tissue from animals untreated or treated with omeprazole or ranitidine. RESULTS: In untreated H. felis-infected animals, the preferred ecological niche was the antrum and cardia equivalent. The density of colonization correlated with the number of parietal cells per gland. Partial acid suppression with ranitidine produced a slight increase in the colonization of the body but was restricted to the upper portions of the gastric gland. Omeprazole treatment produced a greater colonization of the body with bacteria traversing the entire gland. Some reduction in antral colonization occurred. CONCLUSIONS: These results are consistent with the hypothesis that local acid output is a crucial determinant in the distribution of Helicobacter species in the stomach. Differences in local acid output may explain the different patterns of Helicobacter pylori-induced gastric pathology.
BACKGROUND/AIMS: Helicobacter felis colonizes the gastric mucosa of rodents. Preliminary studies showed differences in the distribution of the organism in different parts of the stomach that seemed related to the secretory capacity of the mucosa. The aim of this study was to determine the localization of H. felis in the mouse stomach and to investigate the influence of acid-suppressive agents. METHODS: Specific-pathogen-free BALB/c mice were infected with H. felis. Colonization was assessed in longitudinal sections of gastric tissue from animals untreated or treated with omeprazole or ranitidine. RESULTS: In untreated H. felis-infected animals, the preferred ecological niche was the antrum and cardia equivalent. The density of colonization correlated with the number of parietal cells per gland. Partial acid suppression with ranitidine produced a slight increase in the colonization of the body but was restricted to the upper portions of the gastric gland. Omeprazole treatment produced a greater colonization of the body with bacteria traversing the entire gland. Some reduction in antral colonization occurred. CONCLUSIONS: These results are consistent with the hypothesis that local acid output is a crucial determinant in the distribution of Helicobacter species in the stomach. Differences in local acid output may explain the different patterns of Helicobacter pylori-induced gastric pathology.
Authors: Lucinda J Thompson; Stephen J Danon; John E Wilson; Jani L O'Rourke; Nina R Salama; Stanley Falkow; Hazel Mitchell; Adrian Lee Journal: Infect Immun Date: 2004-08 Impact factor: 3.441
Authors: Sebastian Gehmert; Billie Velapatiño; Phabiola Herrera; Jaqueline Balqui; Livia Santivañez; Jaime Cok; Gloria Vargas; Juan Combe; Douglas J Passaro; Sijin Wen; Frank Meyer; Douglas E Berg; Robert H Gilman Journal: Am J Trop Med Hyg Date: 2009-11 Impact factor: 2.345