ArticlePloS one2012
Helicobacter pylori colonization ameliorates glucose homeostasis in mice through a PPAR γ-dependent mechanism.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Mechanistic Insight into PPARγ and Tregs in Atherosclerotic Immune Inflammation.Frontiers in pharmacology · 2021Review
- The effect ofJournal of diabetes and metabolic disorders · 2020Article
- Identification of new regulatory genes through expression pattern analysis of a global RNA-seq dataset from a Helicobacter pylori co-culture system.Scientific reports · 2020Article
- High-resolution computational modeling of immune responses in the gut.GigaScience · 2019Article
- Interactions between Host PPARs and Gut Microbiota in Health and Disease.International journal of molecular sciences · 2019Review
- The association between Helicobacter pylori seropositivity and risk of new-onset diabetes: a prospective cohort study.Diabetologia · 2018Article
- The Prevalence of Helicobacter pylori in Estonian Bariatric Surgery Patients.International journal of molecular sciences · 2018Article
- Cooperation of Gastric Mononuclear Phagocytes withJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Tissue Tregs.Annual review of immunology · 2016Review
- Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.Gut microbes · 2016Review
- Modeling the Role of Lanthionine Synthetase C-Like 2 (LANCL2) in the Modulation of Immune Responses to Helicobacter pylori Infection.PloS one · 2016Article
- Potential effect of chronic Helicobacter pylori infection on glucose metabolism of Mongolian gerbils.World journal of gastroenterology · 2015Article
- Commensal Streptococcus salivarius Modulates PPARγ Transcriptional Activity in Human Intestinal Epithelial Cells.PloS one · 2015Article
- Modeling the Regulatory Mechanisms by Which NLRX1 Modulates Innate Immune Responses to Helicobacter pylori Infection.PloS one · 2015Article
- Sensitivity Analysis of an ENteric Immunity SImulator (ENISI)-Based Model of Immune Responses to Helicobacter pylori Infection.PloS one · 2015Article
- Beyond the stomach: an updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment.World journal of gastroenterology · 2014Review
- Preclinical studies of amixicile, a systemic therapeutic developed for treatment of Clostridium difficile infections that also shows efficacy against Helicobacter pylori.Antimicrobial agents and chemotherapy · 2014Article
- High-fat maternal diet during pregnancy persistently alters the offspring microbiome in a primate model.Nature communications · 2014Article
- Helicobacter pylori infection in a pig model is dominated by Th1 and cytotoxic CD8+ T cell responses.Infection and immunity · 2013Article
- Mutations to essential orphan response regulator HP1043 of Helicobacter pylori result in growth-stage regulatory defects.Infection and immunity · 2013Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThere is an inverse secular trend between the incidence of obesity and gastric colonization with Helicobacter pylori, a bacterium that can affect the secretion of gastric hormones that relate to energy homeostasis. H. pylori strains that carry the cag pathogenicity island (PAI) interact more intimately with gastric epithelial cells and trigger more extensive host responses than cag(-) strains. We hypothesized that gastric colonization with H. pylori strains differing in cag PAI status exert distinct effects on metabolic and inflammatory phenotypes. METHODOLOGY/PRINCIPAL
findingsTo test this hypothesis, we examined metabolic and inflammatory markers in db/db mice and mice with diet-induced obesity experimentally infected with isogenic forms of H. pylori strain 26695: the cag PAI wild-type and its cag PAI mutant strain 99-305. H. pylori colonization decreased fasting blood glucose levels, increased levels of leptin, improved glucose tolerance, and suppressed weight gain. A response found in both wild-type and mutant H. pylori strain-infected mice included decreased white adipose tissue macrophages (ATM) and increased adipose tissue regulatory T cells (Treg) cells. Gene expression analyses demonstrated upregulation of gastric PPAR γ-responsive genes (i.e., CD36 and FABP4) in H. pylori-infected mice. The loss of PPAR γ in immune and epithelial cells in mice impaired the ability of H. pylori to favorably modulate glucose homeostasis and ATM infiltration during high fat feeding. CONCLUSIONS/SIGNIFICANCE: Gastric infection with some commensal strains of H. pylori ameliorates glucose homeostasis in mice through a PPAR γ-dependent mechanism and modulates macrophage and Treg cell infiltration into the abdominal white adipose tissue.
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