Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in mongolian gerbils

Ohkusa, Toshifumi; Okayasu, Isao; Miwa, Hiroto; Ohtaka, Keiichi; Endo, Shigeru; Sato, Nobuhiro

doi:10.1016/s0016-5085(03)80254-8

Cited by 23 publications

(14 citation statements)

References 28 publications

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“…Gerbils infected with H. pylori develop an antral gastritis/duodenitis that mimics the ulcerogenic form of the human disease (26). Unlike mice but similar to humans, the bacterial cag pathogenicity island seems to be a critical disease determinant in gerbils (27).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori but not High Salt Induces Gastric Intraepithelial Neoplasia in B6129 Mice

et al. 2005

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Helicobacter pylori is responsible for most human stomach cancers. Gastric cancer also is overrepresented in populations consuming high-salt diets. Attempts to test the hypothesis that high salt promotes H. pylori carcinogenesis have been hindered by the lack of a wild-type mouse model. Based on pilot observations of unexpectedly early gastric adenocarcinoma in C57BL/6 Â 129S6/SvEv (B6129) mice infected with Helicobacter felis, we conducted a study to characterize H. pylori infection in these mice and to determine whether high salt promotes tumorigenesis. Male and female mice were gavaged with H. pylori Sydney strain-1 or vehicle only and divided into four groups based on infection status and maintenance on a basal (0.25%) or high (7.5%) salt diet. In uninfected mice, the high-salt diet enhanced proliferation and marginally increased parietal cell mucous metaplasia with oxyntic atrophy. Lesions in H. pylori infected mice without regard to diet or gender were of equivalent severity and characterized by progressive gastritis, oxyntic atrophy, hyperplasia, intestinal metaplasia, and dysplasia. Infected mice on the high-salt diet exhibited a shift in antimicrobial humoral immunity from a Th1 to a Th2 pattern, accompanied by significantly higher colonization and a qualitative increase in infiltrating eosinophils. No mice developed anti-parietal cell antibodies suggestive of autoimmune gastritis. At 15 months of age infected mice in both dietary cohorts exhibited highgrade dysplasia consistent with gastric intraepithelial neoplasia. In summary, we report for the first time H. pylori-induced gastric intraepithelial neoplasia in a wild-type mouse model and show no additive effect of high-salt ingestion on tumor progression. (Cancer Res 2005; 65(23): 10709-15)

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori but not High Salt Induces Gastric Intraepithelial Neoplasia in B6129 Mice

et al. 2005

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“…However, strain SS1 is a mutant of H pylori and its virulence is considerably low. Recently, Mongolian gerbils, which has distinct advantages such as high frequency and stability of infection, large colonization of H pylori, longer living suitable for study with long period of time and pathological changes similar to those observed in human with chronic gastritis, have become the predominant animals for preparing H pylori infection model [42][43][44] . In 1999, Chi et al established a stable model of H pylori infection in Mongolian gerbils, which was orally pretreated with alcohol [49] .…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that infection model in Mongolian gerbils by oral challenge once with H pylori suspension at the concentration of 1×10 8 CFU of H pylori is stable [42][43][44] . In the present study, H pylori was undetectable in the gastric mucosa from Mongolian gerbils at 2 wk after challenge once with 1×10 8 CFU of the bacterium.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, H pylori infection animal models would contribute to screen new drugs against H pylori. In recent published data, Mongolian gerbils have been considered as ideal animals to establish infection model by using internationally collected H pylori strains [42][43][44] . In this study, we used a clinical H pylori isolate named Y06 to establish a stable and reliable infection model in Mongolian gerbils.…”

Section: Introductionmentioning

confidence: 99%

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Establishment ofHelicobacter pyloriinfection model in Mongolian gerbils

Yan¹,

Luo²,

Mao³

2004

WJG

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AIM:To establish a stable and reliable model of Helicobacter pylori infection model in Mongolian gerbils and to observe pathological changes in gastric mucosa in infected animals. METHODS:Mongolian gerbils were randomly divided into 18 groups; 6 groups were infected with H pylori clinical strain Y06 (n=6, groups Y), 6 groups were infected with H pylori strain NCTC11637 (n=6, groups N), and 6 uninfected groups as negative controls (n=4, groups C). H pylori suspensions at the concentrations of 2×10 8 and 2×10 9 CFU/mL of strain NCTC11637 and strain Y06 were prepared. The animals in three groups N and in three groups Y were orally challenged once with 0.5 mL of the low concentration of the bacterial suspension. The animals in another three groups N and in another three groups Y were orally challenged with 0.5 mL of the high concentration of the bacterial suspension for 3 times at the intervals of 24 h, respectively. For the negative controls, the animals in six groups C were orally given w i th t he s am e v ol u m e o f Br u c el l a b r o t h a t t h e corresponding inoculating time. The animals were killed after 2nd, 4 th and 6 th week after the last challenge and the gastric mucosal specimens were taken for urease test, bacterial isolation, pathological and immunohistochemical examinations. RESULTS:Positive isolation rates of H pylori in the animals of groups Y at the 2nd, 4 th and 6 th week after one challenge were 0%, 16.7% and 66.7%, while in the animals of groups N were 0%, 0% and 16.7%, respectively. Positive isolation rates of H pylori in the animals of groups Y at the 2nd, 4 th and 6 th week after three challenges were 66.7%, 100% and 100%, while in the animals of groups N were 66.7%, 66.7% and 100%, respectively. In animals with positive isolation of H pylori, the bacterium was found to colonized on the surface of gastric mucosal cells and in the gastric pits, and the gastric mucosal lamina propria was infiltrated with inflammatory cells.

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“…However, H. pylori infection is still prevalent in developing countries with high infection rates (4). Not only in underdeveloped countries but also in developed countries, H. pylori infection mostly occurs in childhood, and the chances of a new infection are very rare in adulthood (5). In addition, since the probability that H. pylori infection in childhood is naturally healed is extremely low, most infected patients live their life together with the bacteria (6 (6).…”

Section: Introductionmentioning

confidence: 99%

Characterization of Specific IgA Response to Antigenic Determinants ofHelicobacter pyloriUrease Encoded byureAandureBin Children

et al. 2018

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Helicobacter pylori (H. pylori), a causative agent of chronic gastritis and gastric cancer, has several virulent factors for own survival and progression toward gastric diseases in human stomach. Of those, H. pylori produces mainly urease (10~15% total protein weight) that neutralize the gastric acid for survival. Here, we identified the antigenic epitope of urease and then developed an ELISA using the antigen including the epitope of urease. We identified the antigenic epitope of urease that induces IgA antibodies in human using truncated mutants. Eight kinds of seriallytruncated mutant of UreA and UreB were prepared and subjected to immunoblot using pooled sera of patients with gastric disorders. UreBEnd protein containing UreB epitope was produced and investigated its diagnostic value via ELISA in children. As a result, mutants having last 24 amino acid residues of UreB carboxyl terminus deleted did not show IgA-reactive band.

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Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in mongolian gerbils

Cited by 23 publications

References 28 publications

Helicobacter pylori but not High Salt Induces Gastric Intraepithelial Neoplasia in B6129 Mice

Helicobacter pylori but not High Salt Induces Gastric Intraepithelial Neoplasia in B6129 Mice

Establishment ofHelicobacter pyloriinfection model in Mongolian gerbils

Characterization of Specific IgA Response to Antigenic Determinants ofHelicobacter pyloriUrease Encoded byureAandureBin Children

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