Helicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanism

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dc.contributor.authorBassaganya-Riera, Josepen
dc.contributor.authorDominguez-Bello, Maria Gloriaen
dc.contributor.authorKronsteiner, Barbaraen
dc.contributor.authorCarbo, Adriaen
dc.contributor.authorPinyi, Luen
dc.contributor.authorViladomiu, Monicaen
dc.contributor.authorPedragosa, Mireiaen
dc.contributor.authorZhang, Xiaoyingen
dc.contributor.authorSobral, Brunoen
dc.contributor.authorMane, Shrinivasrao P.en
dc.contributor.authorMohapatra, Saroj K.en
dc.contributor.authorHorne, William T.en
dc.contributor.authorGuri, Amir J.en
dc.contributor.authorGroeschl, Michaelen
dc.contributor.authorLopez-Velasco, Gabrielaen
dc.contributor.authorHontecillas, Raquelen
dc.date.accessed2014-04-29en
dc.date.accessioned2014-06-17T20:12:08Zen
dc.date.available2014-06-17T20:12:08Zen
dc.date.issued2012-11-15en
dc.description.abstractBackground: There 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 Findings: To 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.en
dc.description.sponsorshipThis study was supported in part by the National Institutes of Health 5R01AT004308 to JB-R, National Institute of Allergy and Infectious Diseases contract number HHSN272201000056C to JB-R, National Institute of Allergy and Infectious Diseases contract number HHSN272200900040C to BWS, Virginia Bioinformatics Institute (VBI) exploratory grant (JB-R). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en
dc.identifier.citationBassaganya-Riera J, Dominguez-Bello MG, Kronsteiner B, Carbo A, Lu P, et al. (2012) Helicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanism. PLoS ONE 7(11): e50069. doi:10.1371/journal.pone.0050069en
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0050069en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://hdl.handle.net/10919/49001en
dc.identifier.urlhttp://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0050069en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectGastgrointestinal infectionsen
dc.subjectGlucoseen
dc.subjectHelicobacter pylorien
dc.subjectInflammationen
dc.subjectLeptinen
dc.subjectMacrophagesen
dc.subjectObesityen
dc.subjectTrophic interactionsen
dc.titleHelicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanismen
dc.title.serialPLoS ONEen
dc.typeArticle - Refereeden

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