H Miyata, K Yagi, M Kimura, H Kijima, Y Isobe, Y Kaneda, T Akashi
{"title":"Distribution of Helicobacter pylori in a Mongolian gerbil gastric ulcer model.","authors":"H Miyata, K Yagi, M Kimura, H Kijima, Y Isobe, Y Kaneda, T Akashi","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and purpose: </strong>To the authors' knowledge, histopathologic changes associated with early H. pylori infection and ulceration have not been established. We examined presence of H. pylori infection in an acetic acid-induced gastric ulcer (AAU) model in Mongolian gerbils.</p><p><strong>Methods: </strong>Sixty Mongolian gerbils were used as an AAU model, and another 60 gerbils were studied as a control (non-AAU) group. All animals were orally administered H. pylori, then were evaluated by use of histologic and bacteriologic examinations.</p><p><strong>Results: </strong>Helicobacter pylori were scattered on the surface mucous gel layer and in the pyloric gland gastric were pits; inflammation seen at the early stages later extended to the mucosa of the fundic gland area. The organisms were predominantly observed in the AAU model, but findings were comparable to those in controls at 1, 3, 7, 14, 28, or 56 days. Evaluation with regard to viable bacterial numbers reflected the histologic aspects, that the pyloric gland area had more viable counts than did the fundic gland area. Carbohydrate composition of mucin differed between pyloric and fundic gland areas. These findings shed light on L-fucose related to the H. pylori adhesive factor abundant in mucin of the pyloric gland area.</p><p><strong>Conclusions: </strong>Findings for this ulcer model of Helicobacter pylori infection make it useful for the study of onset of infection and screening of anti-ulcer agents.</p>","PeriodicalId":17937,"journal":{"name":"Laboratory animal science","volume":"49 6","pages":"622-7"},"PeriodicalIF":0.0000,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Laboratory animal science","FirstCategoryId":"3","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background and purpose: To the authors' knowledge, histopathologic changes associated with early H. pylori infection and ulceration have not been established. We examined presence of H. pylori infection in an acetic acid-induced gastric ulcer (AAU) model in Mongolian gerbils.
Methods: Sixty Mongolian gerbils were used as an AAU model, and another 60 gerbils were studied as a control (non-AAU) group. All animals were orally administered H. pylori, then were evaluated by use of histologic and bacteriologic examinations.
Results: Helicobacter pylori were scattered on the surface mucous gel layer and in the pyloric gland gastric were pits; inflammation seen at the early stages later extended to the mucosa of the fundic gland area. The organisms were predominantly observed in the AAU model, but findings were comparable to those in controls at 1, 3, 7, 14, 28, or 56 days. Evaluation with regard to viable bacterial numbers reflected the histologic aspects, that the pyloric gland area had more viable counts than did the fundic gland area. Carbohydrate composition of mucin differed between pyloric and fundic gland areas. These findings shed light on L-fucose related to the H. pylori adhesive factor abundant in mucin of the pyloric gland area.
Conclusions: Findings for this ulcer model of Helicobacter pylori infection make it useful for the study of onset of infection and screening of anti-ulcer agents.