ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2011
Helicobacter felis--associated gastric disease in microbiota-restricted mice.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Interplay and cooperation of Helicobacter pylori and gut microbiota in gastric carcinogenesis.BMC microbiology · 2021Review
- Review
- Oral microbiota and Helicobacter pylori in gastric carcinogenesis: what do we know and where next?BMC microbiology · 2021Review
- Review
- In-feed bambermycin medication induces anti-inflammatory effects and prevents parietal cell loss without influencing Helicobacter suis colonization in the stomach of mice.Veterinary research · 2018Article
- The Altered Schaedler Flora: Continued Applications of a Defined Murine Microbial Community.ILAR journal · 2015Review
- Human pharyngeal microbiome may play a protective role in respiratory tract infections.Genomics, proteomics & bioinformatics · 2014Article
- Consumption of acidic water alters the gut microbiome and decreases the risk of diabetes in NOD mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
- Article
- Gut Microbiota and Obesity.Current obesity reports · 2012Article
- Article
- Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Human Helicobacter pylori infection leads to multiple pathological consequences, including gastritis and adenocarcinoma. Although this association has led to the classification of H. pylori as a type 1 carcinogen, it is not clear if additional nonhelicobacter gastric microbiota play a role in these diseases. In this study, we utilized either specific pathogen-free C57BL/6 mice (B6.SPF) or mice colonized with altered Schaedler flora (B6.ASF) to evaluate the role of nonhelicobacter gastric microbiota in disease development after Helicobacter felis infection. Despite similar histological changes, H. felis persisted in B6.ASF stomachs, while H. felis could no longer be detected in the majority of B6.SPF mice. The B6.SPF mice also acquired multiple Lactobacillus spp. in their stomachs after H. felis infection. Our data indicate that potential mechanisms responsible for the ineffective H. felis clearance in the B6.ASF model include the absence of new gastric microbiota to compete for the gastric niche, the lack of expression of new gastric mucins, and a reduced ratio of H. felis-specific IgG2c:IgG1 serum antibodies. These data suggest that although H. felis is sufficient to initiate gastric inflammation and atrophy, bacterial eradication and the systemic immune response to infection are significantly influenced by pre-existing and acquired gastric microbiota.
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Registered trials
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.