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PLoS One. 2014 Apr 7;9(4):e94209. doi: 10.1371/journal.pone.0094209. eCollection 2014.

The role of estrogen signaling in a mouse model of inflammatory bowel disease: a Helicobacter hepaticus model.

Author information

  • 1Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, United States of America.
  • 2Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, United States of America; Department of Molecular Microbiology & Immunology, University of Missouri, Columbia, Missouri, United States of America.
  • 3Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, United States of America; IDEXX Laboratories, Columbia, Missouri, United States of America.
  • 4Department of Biochemistry, University of Missouri, Columbia, Missouri, United States of America.
  • 5Departments of Health Management and Informatics, and Statistics, University of Missouri, Columbia, Missouri, United States of America.

Abstract

The pathogenesis of inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, is due in part to interactions between the immune system, genetics, the environment, and endogenous microbiota. Gonadal sex hormones (GSH), such as estrogen, are thought to be involved in the development of IBD as variations in disease severity occur during pregnancy, menopause, or oral contraceptives use. In certain strains of mice, infection with Helicobacter hepaticus triggers IBD-like mucosal inflammation that is more severe in female mice than in males, suggesting a role for GSH in this model. To determine the role of estrogen signaling in microbiota-induced intestinal inflammation, estrogen receptor (ER) α and β knock-out (KO) mice, ER agonists, and adoptive transfers were utilized. We demonstrate that, when signaling is limited to ERβ on a non-CD4+ cell subset, disease is less severe and this correlates with decreased expression of pro-inflammatory mediators.

PMID:
24709804
[PubMed - indexed for MEDLINE]
PMCID:
PMC3978010
Free PMC Article
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