Helicobacter pylori infection induces gastric cancer in Mongolian gerbils

Watanabe, Takeshi; Tada, Mitsuru; Nagai, Hirofumi; Sasaki, Satoshi; Nakao, Megumi

doi:10.1016/s0021-5198(19)34094-6

Cited by 27 publications

(38 citation statements)

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“…Furthermore, WT-infected animals revealed an increased carcinoma risk index [22] as compared to the mutant-infected ones, but none of the infected gerbils developed gastric adenocarcinoma. Our data are in agreement with several studies of western research groups [7] , [34] , but contradicting published data from Japanese groups and others, that demonstrated a H. pylori -induced gastric cancer in Mongolian gerbils [16] , [35] , [36] . Thus, our data support a multifactorial process of gastric cancer induction, as it is suggested to occur in humans.…”

Section: Discussionsupporting

confidence: 84%

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Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils

et al. 2009

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Infection with Helicobacter pylori, carrying a functional cag type IV secretion system (cag-T4SS) to inject the Cytotoxin associated antigen (CagA) into gastric cells, is associated with an increased risk for severe gastric diseases in humans. Here we studied the pathomechanism of H. pylori and the role of the cag-pathogenicity island (cag-PAI) for the induction of gastric ulcer and precancerous conditions over time (2–64 weeks) using the Mongolian gerbil model. Animals were challenged with H. pylori B128 (WT), or an isogenic B128ΔcagY mutant-strain that produces CagA, but is unable to translocate it into gastric cells. H. pylori colonization density was quantified in antrum and corpus mucosa separately. Paraffin sections were graded for inflammation and histological changes verified by immunohistochemistry. Physiological and inflammatory markers were quantitated by RIA and RT-PCR, respectively. An early cag-T4SS-dependent inflammation of the corpus mucosa (4–8 weeks) occurred only in WT-infected animals, resulting in a severe active and chronic gastritis with a significant increase of proinflammatory cytokines, mucous gland metaplasia, and atrophy of the parietal cells. At late time points only WT-infected animals developed hypochlorhydria and hypergastrinemia in parallel to gastric ulcers, gastritis cystica profunda, and focal dysplasia. The early cag-PAI-dependent immunological response triggers later physiological and histopathological alterations towards gastric malignancies.

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Section: Discussionsupporting

confidence: 84%

“…It could be shown that infection of wild-type mice with cag + strains frequently leads to deletions within the cag -PAI [14] , [15] . Therefore, the Mongolian gerbil model has been established to study H. pylori pathogenesis towards gastric adenocarcinoma [16] .…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils

et al. 2009

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“…Interstitial cell tumours are well documented in the testicle of domestic, laboratory and exotic animal species, whereas the neoplasm infrequently arises in the ovary. Mongolian gerbils have been used as laboratory subjects for evaluation of Helicobacter‐induced gastric carcinomas and ischaemic brain injury due to similarities in these disease processes to human patients (Levine and Payan 1966, Watanabe and others 1998) and have also become popular as pets. Neoplasms of aged gerbils are among the most commonly reported diseases (Rowe and others 1974).…”

Section: Introductionmentioning

confidence: 99%

Ovarian interstitial cell tumour in a Mongolian gerbil (Meriones unguiculatus)

Kubiak

Jayson

Denk

2015

Vet Record Case Reports

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A 22-month-old female Mongolian gerbil presented with palpable cranial abdominal masses. At initial presentation, no clinical signs were associated with the masses and the owner elected to monitor the gerbils’ condition. Abdominal distention developed over the following eight months and was progressively associated with altered demeanour, reduced mobility and increased respiratory effort. An exploratory laparotomy identified left-sided ovarian masses and right-sided ovarian cysts. A bilateral ovariectomy was performed. No other changes were noted. Recovery from surgery was uneventful, but the gerbil died six weeks later. Histological findings were consistent with a unilateral ovarian interstitial cell tumour accompanied by contralateral ovarian cysts and interstitial cell hyperplasia. To the authors’ knowledge, this is the first report of an ovarian interstitial cell tumour in a Mongolian gerbil.

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“…31). Mongolian gerbils infected with CagA-positive H. pylori have been reported to develop gastric dysplasia and even gastric cancer (Refs 32, 33). However, it remains controversial whether the lesions described are actually cancers; the majority of laboratories have been unable to confirm development of cancer (Refs 31, 34, 35) despite use of the same strains of H. pylori and long periods of observation (Refs 34, 35).…”

Section: Caga As a Risk Factor And As An Oncoproteinmentioning

confidence: 99%

Helicobacter pylorias an oncogenic pathogen, revisited

Miftahussurur¹,

Yamaoka²,

Graham³

2017

Expert Rev. Mol. Med.

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Gastric cancer is an inflammation-associated malignancy aetiologically related to infection with the bacterium, Helicobacter pylori, which is considered a necessary but insufficient cause. Unless treated, H. pylori causes life-long acute and chronic gastric inflammation resulting in progressive gastric mucosal damage that may result in gastric cancer. The rate of progression from superficial gastritis, to an atrophic metaplastic mucosa, and ultimately to cancer relates to the virulence of the infecting H. pylori as well as host and environmental factors. H. pylori virulence is a reflection of its propensity to cause severe gastric inflammation. Both mucosal inflammation and H. pylori can cause host genomic instability, including dysregulation of DNA mismatch repair, stimulation of expression of activation-induced cytidine deaminase, abnormal DNA methylation and dysregulation of micro RNAs, which may result in an accumulation of mutations and loss of normal regulation of cell growth. The difference in cancer risk between the most and least virulent H. pylori strain is only approximately 2-fold. Overall, none of the putative virulence factors identified to date have proved to be disease-specific. The presence, severity, extent and duration of inflammation appear to be the most important factors and current evidence suggests that any host, environmental or bacterial factor that reliably enhances the inflammatory response to the H. pylori infection increases the risk of gastric cancer.

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Helicobacter pylori infection induces gastric cancer in Mongolian gerbils

Cited by 27 publications

References 0 publications

Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils

Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils

Ovarian interstitial cell tumour in a Mongolian gerbil (Meriones unguiculatus)

Helicobacter pylorias an oncogenic pathogen, revisited

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