p27kip1 Deficiency Confers Susceptibility to Gastric Carcinogenesis in Helicobacter pylori–Infected Mice

Kuzushita, Noriyoshi; Rogers, Arlin B.; Monti, Nola A.; Whary, Mark T.; Park, Min J.; Aswad, Bassam I.; Shirin, Haim; Koff, Andrew; Eguchi, Hidetoshi; Moss, Steven F.

doi:10.1053/j.gastro.2005.07.056

Cited by 50 publications

(47 citation statements)

References 55 publications

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“…H. pylori infection has been associated with increased IL-8 expression and decreased p27 levels (64). Both reduced p27 levels and increased IL-8 levels have been shown to mediate decreased apoptosis (65)(66)(67)(68). When exposed to morevirulent European strains expressing higher levels of cagA, gastric epithelial cells increased IL-8 expression, which promotes the activation and infiltration of inflammatory cells and the reduction of apoptosis.…”

Section: Origin Alters Transcription and Virulence Of H Pylorimentioning

confidence: 99%

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

et al. 2013

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g While Helicobacter pylori infects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host, and environmental factors play a role in disease outcome. To investigate the role of bacterial factors in H. pylori pathogenesis, global gene expression of six H. pylori isolates was analyzed during coculture with gastric epithelial cells. Clustering analysis of six Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk segregated strains based on their phylogeographic origin. One hundred forty-six genes had increased expression in European strains, while 350 genes had increased expression in African strains. Differential expression was observed in genes associated with motility, pathogenicity, and other adaptations to the host environment. European strains had greater expression of the virulence factors cagA, vacA, and babB and were associated with increased gastric histologic lesions in patients. In AGS cells, European strains promoted significantly higher interleukin-8 (IL-8) expression than did African strains. African strains significantly induced apoptosis, whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and that these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that bacterial factors determined by the phylogeographic origin of H. pylori strains may promote increased gastric disease.

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Section: Origin Alters Transcription and Virulence Of H Pylorimentioning

confidence: 99%

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

et al. 2013

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“…However, most in vitro studies have shown the opposite result, that is, apoptosis prevails rather than proliferation after H. pylori or its supernatants treatment. Therefore, it is suggested that increased cell proliferation in gastric epithelium in vivo might be an indirect or secondary response to H. pylori infection [43][44][45]. Together with the previous publications that suppressed apoptosis might be one of major pathogenic factors in H. pylori-associated carcinogenesis [46][47][48] and oncogenic stem cells contributed to H. pylori-associated carcinogenesis [49], we could conclude that the reemergence of Shh expressing cells can explain these compensatory or counteractive privileges of proliferation through imbalanced epithelial turnover and this anti-apoptotic steps and proliferative privileges through Shh reactivation could be the necessary path for H. pylori-associated carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Late reactivation of sonic hedgehog by Helicobacter pylori results in population of gastric epithelial cells that are resistant to apoptosis: Implication for gastric carcinogenesis

Lee¹,

Lee²,

Jung³

et al. 2010

Cancer Letters

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“…Additionally, p27-defi cient mice easily developed tumors when exposed to environmental carcinogenic agents [ 50 ]. In a 60-week observational sturdy, p27-defi cient mice infected with H. pylori SS1 developed metaplasia, dysplasia, and gastric cancer [ 51 ].…”

Section: P27-defi Cient Micementioning

confidence: 99%

Animal Models of H. pylori Infection

Lee

2016

Helicobacter Pylori

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The best suited animal models of Helicobacter pylori ( H. pylori ) identifi ed so far are rodents. Helicobacter felis infection provokes severe infl ammation and induces well sequential carcinogenic events leading to dysplasia and gastric adenocarcinoma. H. pylori SS1 is the most useful strain identifi ed so far. It expresses cytotoxin-associated gene A ( cagA ) and vacuolating cytotoxin ( vacA ) and can easily colonize the stomach of mice and induce humanlike gastric pathological changes. However, a long-term colonization of the stomach does not always induce dysplasia or adenocarcinoma. Unlike H. pylori SS1, however, it lacks the cag pathogenicity island (PAI) and does not adhere well to gastric epithelial cells. Individuals colonized by the same strain show different responses. This is ascribable to T cell immune responses, whereby the balance between the immune responses of Th1 and Th2 plays an important role. A variety of transgenic or knockout mice have been developed and used. Such animal models have greatly contributed to identifying immunophysiology associated with H. pylori .

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p27kip1 Deficiency Confers Susceptibility to Gastric Carcinogenesis in Helicobacter pylori–Infected Mice

Cited by 50 publications

References 55 publications

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

Late reactivation of sonic hedgehog by Helicobacter pylori results in population of gastric epithelial cells that are resistant to apoptosis: Implication for gastric carcinogenesis

Animal Models of H. pylori Infection

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