Hepato-gastroenterology · 2001
Effect of Helicobacter pylori culture supernatant on acute reflux esophagitis in a rat model.
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Fujiwara Y, Higuchi K, Tominaga K, Matsuo T, Watanabe T, Uchida T, Saeki Y, Arakawa T, Tarnawski A
Аннотация
BACKGROUND/AIMS: Prevalence of Helicobacter pylori, especially cagA-positive strains is inversely related to gastroesophageal reflux disease. The aim of this study was to examine whether H. pylori culture supernatants affect acute esophagitis induced by acid or mixed reflux in rats.
METHODOLOGY: Three different H. pylori strains were used. Acute esophagitis was induced in 59 male Wistar rats by ligation of both the transitional regions between the forestomach and glandular portion, and the pylorus or the lower part of duodenum. After operation, the rats were either left untreated or treated with intragastric injection of either vehicle or H. pylori culture supernatants and were sacrificed 6 or 24 hours later. Esophagitis index, depth of esophageal lesions, esophageal epithelial degeneration, and infiltration of inflammatory cells were examined.
RESULTS: Gross esophageal erosions and ulcers were observed up to mid-esophagus in all animals. H. pylori culture supernatants did not affect esophageal mucosal injury and no histologically significant differences were found among rats.
CONCLUSIONS: H. pylori culture supernatants, regardless of cagA gene expression, did not affect acute esophagitis induced by acid or mixed reflux. This finding suggests that no powerful protective factors against reflux-induced mucosal injury were produced by H. pylori.
METHODOLOGY: Three different H. pylori strains were used. Acute esophagitis was induced in 59 male Wistar rats by ligation of both the transitional regions between the forestomach and glandular portion, and the pylorus or the lower part of duodenum. After operation, the rats were either left untreated or treated with intragastric injection of either vehicle or H. pylori culture supernatants and were sacrificed 6 or 24 hours later. Esophagitis index, depth of esophageal lesions, esophageal epithelial degeneration, and infiltration of inflammatory cells were examined.
RESULTS: Gross esophageal erosions and ulcers were observed up to mid-esophagus in all animals. H. pylori culture supernatants did not affect esophageal mucosal injury and no histologically significant differences were found among rats.
CONCLUSIONS: H. pylori culture supernatants, regardless of cagA gene expression, did not affect acute esophagitis induced by acid or mixed reflux. This finding suggests that no powerful protective factors against reflux-induced mucosal injury were produced by H. pylori.