ArticleProceedings of the National Academy of Sciences of the United States of America2010
Mutagenic potency of Helicobacter pylori in the gastric mucosa of mice is determined by sex and duration of infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Mucosal Inducible NO Synthase-Producing IgA+ Plasma Cells in Helicobacter pylori-Infected Patients.Journal of immunology (Baltimore, Md. : 1950) · 2016Trial
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Helicobacter pylori-Induced Host Cell DNA Damage and Genetics of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- Review
- Glucocorticoids and Androgens Protect From Gastric Metaplasia by Suppressing Group 2 Innate Lymphoid Cell Activation.Gastroenterology · 2021Article
- Article
- Interleukin-21 (IL-21) Downregulates Dendritic Cell Cytokine Responses to Helicobacter pylori and Modulates T Lymphocyte IL-17A Expression in Peyer's Patches during Infection.Infection and immunity · 2019Article
- Mutagenicity of Helicobacter hepaticus infection in the lower bowel mucosa of 129/SvEv Rag2International journal of cancer · 2019Article
- Helicobacter pylori-infected C57BL/6 mice with different gastrointestinal microbiota have contrasting gastric pathology, microbial and host immune responses.Scientific reports · 2018Article
- Oxidative Stress Resulting FromCellular and molecular gastroenterology and hepatology · 2017Review
- Fas-associated factor 1 inhibits tumor growth by suppressing Helicobacter pylori-induced activation of NF-κB signaling in human gastric carcinoma.Oncotarget · 2017Article
- Article
- Intrinsic mutagenic properties of 5-chlorocytosine: A mechanistic connection between chronic inflammation and cancer.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Helicobacter cinaedi induced typhlocolitis in Rag-2-deficient mice.Helicobacter · 2015Article
- Inflammation-induced cell proliferation potentiates DNA damage-induced mutations in vivo.PLoS genetics · 2015Article
- Helminth co-infection in Helicobacter pylori infected INS-GAS mice attenuates gastric premalignant lesions of epithelial dysplasia and glandular atrophy and preserves colonization resistance of the stomach to lower bowel microbiota.Microbes and infection · 2014Article
- Serum Helicobacter pylori CagA antibody titer as a useful marker for advanced inflammation in the stomach in Japan.Journal of gastroenterology and hepatology · 2014Article
- Chemistry meets biology in colitis-associated carcinogenesis.Free radical research · 2013Review
- S-nitrosoglutathione reductase deficiency increases mutagenesis from alkylation in mouse liver.Carcinogenesis · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori is a human carcinogen, but the mechanisms evoked in carcinogenesis during this chronic inflammatory disease remain incompletely characterized. We determined whether chronic H. pylori infection induced mutations in the gastric mucosa of male and female gpt delta C57BL/6 mice infected for 6 or 12 mo. Point mutations were increased in females infected for 12 mo. The mutation frequency in this group was 1.6-fold higher than in uninfected mice of both sexes (P < 0.05). A:T-to-G:C transitions and G:C-to-T:A transversions were 3.8 and 2.0 times, respectively, more frequent in this group than in controls. Both mutations are consistent with DNA damage induced by oxidative stress. No increase in the frequency of deletions was observed. Females had more severe gastric lesions than males at 6 mo postinfection (MPI; P < 0.05), but this difference was absent at 12 MPI. In all mice, infection significantly increased expression of IFNgamma, IL-17, TNFalpha, and iNOS at 6 and 12 mo, as well as H. pylori-specific IgG1 levels at 12 MPI (P < 0.05) and IgG2c levels at 6 and 12 MPI (P < 0.01 and P < 0.001). At 12 MPI, IgG2c levels in infected females were higher than at 6 MPI (P < 0.05) and also than those in infected males at 12 MPI (P < 0.05). Intensity of responses was mediated by sex and duration of infection. Lower H. pylori colonization indicated a more robust host response in females than in males. Earlier onset of severe gastric lesions and proinflammatory, Th1-biased responses in female C57BL/6 mice may have promoted mutagenesis by exposing the stomach to prolonged oxidative stress.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.