Inflammation and Cancer I. Rodent models of infectious gastrointestinal and liver cancer

Rogers, Arlin B.; Fox, James G.

doi:10.1152/ajpgi.00499.2003

Cited by 112 publications

(103 citation statements)

References 20 publications

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“…The combination of these effects could be beneficial for cell survival in the early phase of the infection. The sustained overproduction of IL-6 and anti-apoptotic proteins Bcl-2 and Bcl-XL facilitates proliferation of the inflamed cells, thereby promoting the development of pre-malignant dysplastic lesions that ultimately give rise to cancer (47,48). In the ceca of H.japonicum infected mice, the γ-H2AX staining, the marker for DNA DSBs, was significantly increased when compared with control ceca.…”

Section: Discussionmentioning

confidence: 99%

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice

Shen¹,

Feng²,

Muthupalani³

et al. 2016

CARCIN

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A novel Helicobacter species Helicobacter japonicum was isolated from the stomach and intestines of clinically normal mice received from three institutes from Japan. The novel Helicobacter sp. was microaerobic, grew at 37°C and 42°C, was catalase and oxidase positive, but urease negative. It is most closely related to the 16S rRNA gene of H.muridarum (98.6%); to the 23S rRNA gene of H.hepaticus (97.9%); to the hsp60 gene of H.typhlonius (87%). The novel Helicobacter sp. has in vitro cytolethal distending toxin (CDT) activity; its cdtB gene sequence has 83.8% identity with that of H.hepaticus. The whole genome sequence of H.japonicum MIT 01-6451 has a 2.06-Mb genome length with a 37.5% G + C content. When the organism was inoculated into C57BL/129 IL10 −/− mice, it was cultured from the stomach, colon and cecum of infected mice at 6 and 10 weeks post-infection. The cecum had the highest H.japonicum colonization levels by quantitative PCR. The histopathology of the lower bowel was characterized by moderate to severe inflammation, mild edema, epithelial defects, mild to severe hyperplasia, dysplasia and carcinoma. Inflammatory cytokines IFNγ, TNFα and IL17a, as well as iNOS were significantly upregulated in the cecal tissue of infected mice. These results demonstrate that the novel H.japonicum can induce inflammatory bowel disease and carcinoma in IL10 −/− mice and highlights the importance of identifying novel Helicobacter spp. especially when they are introduced from outside mouse colonies from different geographic locations.

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Section: Discussionmentioning

confidence: 99%

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice

Shen¹,

Feng²,

Muthupalani³

et al. 2016

CARCIN

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“…17 Cao et al 23 reported that antimicrobial therapy induces apoptosis and inhibits proliferation in H. pylori-infected gerbil gastric mucosa. However, the effect of H. pylori eradication on pre-malignant (eg, dysplasia) and malignant histological lesions was not examined.…”

Section: Discussionmentioning

confidence: 99%

“…17 Long-term (41 year) H. pylori infection of Mongolian gerbils can lead to gastric adenocarcinoma, without the coadministration of carcinogens, and gastric cancer in this model occurs in the distal stomach, as in humans. [18][19][20] However, before 2005, the development of gastric cancer in gerbils had never been demonstrated outside east Asia, which limited the widespread use of this model.…”

mentioning

confidence: 87%

Effect of Helicobacter pylori eradication on gastric carcinogenesis

Romero–Gallo

Harris

Krishna

et al. 2008

Laboratory Investigation

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Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, yet the effects of bacterial eradication on carcinogenesis remain unclear. Animal models provide important insights into factors that are involved in gastric carcinogenesis, and we previously utilized such a model to demonstrate that an in vivoadapted H. pylori strain, 7.13, rapidly and reproducibly induces inflammation-mediated gastric carcinoma. In the current study, we used this bacterial strain as a prototype to define the role of targeted antimicrobial therapy in gastric carcinogenesis. Mongolian gerbils were infected with H. pylori for 4 or 8 weeks, treated with antimicrobial agents or vehicle, and then euthanized at 8 weeks after the completion of therapy. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals receiving antimicrobial therapy. Gastric dysplasia or cancer developed in 460% of the gerbils that remained persistently colonized with H. pylori, but in none of the animals treated with antibiotics following 4 weeks of infection. Infection with H. pylori for 8 weeks prior to therapy resulted in an attenuation, but not complete prevention, of pre-malignant and malignant lesions. Similarly, antibiotic therapy initiated at 4, but not 8, weeks after H. pylori challenge significantly reduced expression of the Th1 pro-inflammatory cytokine interferon-g within colonized gastric mucosa. These results indicate that treatment of H. pylori in this model decreases the incidence and severity of lesions with carcinogenic potential. The effectiveness of eradication is dependent upon the timing of intervention, providing insights into mechanisms that may regulate the development of malignancies arising within the context of inflammatory states.

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“…However, the primary habitat of H. hepaticus is the intestinal tract and the bacterium is linked to inflammatory bowl disease in immunocompromised mice. Recent studies showed that H. hepaticus infected mice might serve as an ideal animal model to study inflammation related carcinogenesis in humans [2,3]. The annotated genome sequence of H. hepaticus has been published [4].…”

Section: Introductionmentioning

confidence: 99%

The NADPH quinone reductase MdaB confers oxidative stress resistance to Helicobacter hepaticus

Yang

Wang

Maier

2008

Microbial Pathogenesis

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An mdaB mutant strain in a quinone reductase (MdaB) of Helicobacter hepaticus type strain ATCC51449 was constructed by insertional mutagenesis, and the MdaB protein was purified and compared to the Helicobacter pylori enzyme. While wild type H. hepaticus cells could tolerate 6% O 2 for growth, the mdaB strain was clearly inhibited at this oxygen level. Disruption of the gene downstream of mdaB (HH1473) did not affect the oxidative stress phenotype of the strain. The mdaB mutant was also more sensitive to oxidative stress reagents such as H 2 O 2 , cumene hydroperoxide, t-butyl hydroperoxide, and paraquat. All H. hepaticus mdaB strains isolated constitutively up-expressed another oxidative stress combating enzyme, superoxide dismutase; this is in contrast to H. pylori mdaB strains. H. hepaticus MdaB is a flavoprotein catalyzing quinone reduction using a two-electron transfer mechanism from NAD(P)H to quinone. The H. hepaticus enzyme specific activity was far less than for the H. pylori enzyme purified in the same manner.

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Inflammation and Cancer I. Rodent models of infectious gastrointestinal and liver cancer

Cited by 112 publications

References 20 publications

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice

Effect of Helicobacter pylori eradication on gastric carcinogenesis

The NADPH quinone reductase MdaB confers oxidative stress resistance to Helicobacter hepaticus

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Inflammation and Cancer I. Rodent models of infectious gastrointestinal and liver cancer

Cited by 112 publications

References 20 publications

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10−/−mice

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10−/−mice

Effect of Helicobacter pylori eradication on gastric carcinogenesis

The NADPH quinone reductase MdaB confers oxidative stress resistance to Helicobacter hepaticus

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NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice

NovelHelicobacterspeciesH.japonicumisolated from laboratory mice from Japan induces typhlocolitis and lower bowel carcinoma in C57BL/129 IL10^−/−mice