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Home › Dataset Library › Helicobacter pylori colonization ameliorates glucose homeostasis in mice

Dataset: Helicobacter pylori colonization ameliorates glucose homeostasis in mice

Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-...

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Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-positive H. pylori strains interact intimately with the host gastric epithelial cells and trigger higher inflammation than cag-negative strains, we hypothesized that gastric colonization with H. pylori strains without functional cagA ameliorates obesity and its complications by modulating gastric gene expression and inflammation. Methodology/Principal Findings: To test this hypothesis we examined the effects of gastric colonization on metabolic and inflammatory markers in mice infected with two isogenic strains of H. pylori: 26695 strain 98-325 (cagA+ wild-type) and its cag pathogenicity island (cagPAI) mutant strain 99-305, a knockout made by inserting a chloramphenicol resistance cassette. Only the cagPAI mutant decreased fasting blood glucose levels, improved glucose tolerance and suppressed weight gain in db/db mice and mice with diet-induced obesity. These effects were associated with increased gastric leptin levels, suppressed infiltration of macrophages, enhanced influx of regulatory T cells (Treg) in adipose tissue and suppressed gastric inflammation. Gene set enrichment analyses of gastric mucosal samples identified six differentially modulated pathways, including the Hedgehog signaling pathway that is associated with control of cellular proliferation and gastric carcinogenesis as well as the insulin signaling pathway. Conclusions/Significance: Gastric colonization with cagPAI-negative strains of H. pylori ameliorate obesity and inflammation by modulating gastric gene expression, suggesting that cag-negative H. pylori strains might be beneficial in ameliorating obesity and its co-morbidities. Gastric mucosa from three groups of mice: uninfected, infected with H. pylori 26695 strain 98-325 (cagA+ wild-type) or infected with H. pylori mutant strain 99-305 (lacking cag pathogenicity island; cagA-)

Species:
mouse

Samples:
9

Source:
E-GEOD-21833

Updated:
Dec.12, 2014

Registered:
Nov.11, 2014


Factors: (via ArrayExpress)
Sample INFECTION
GSM543406 uninfected
GSM543406 uninfected
GSM543406 uninfected
GSM543409 H. pylori strain 99-305 (mutant, HpcagA-)
GSM543409 H. pylori strain 99-305 (mutant, HpcagA-)
GSM543409 H. pylori strain 99-305 (mutant, HpcagA-)
GSM543412 H. pylori strain 98-325 (wild-type, HpcagA+)
GSM543412 H. pylori strain 98-325 (wild-type, HpcagA+)
GSM543412 H. pylori strain 98-325 (wild-type, HpcagA+)

Tags

  • adipose tissue
  • body
  • glucose
  • insulin
  • mucosa
  • obesity

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