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Impaired expression of peroxisome proliferator-activated receptor gamma in ulcerative colitis

Laurent Dubuquoy1, Emmelie A Jansson, Samir Deeb

  • 1Equipe Propre INSERM 0114 sur la Physiopathologie des Maladies Inflammatoires Intestinales, Lille, France.

Gastroenterology
|May 6, 2003
PubMed
Abstract

Insights

Intestinal bacteria influence PPAR gamma expression, which is reduced in ulcerative colitis patients. This finding highlights the role of gut microbiota in inflammatory bowel disease pathogenesis.

Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiology

Background:

  • Peroxisome proliferator-activated receptor gamma (PPAR gamma) may inhibit colitis by reducing nuclear factor kappa B (NF-kappa B) activity.
  • Elevated NF-kappa B activators, such as toll-like receptor 4 (TLR4), are implicated in inflammatory bowel disease (IBD).

Purpose of the Study:

  • To investigate the influence of bacteria and their signaling pathways on PPAR gamma regulation in IBD.
  • To assess the role of TLR4 in PPAR gamma expression within the context of IBD.

Main Methods:

  • Assessed PPAR gamma expression in TLR4-transfected Caco-2 cells, germ-free mice, and TLR4-deficient mice (Lps(d)/Lps(d)).
  • Evaluated colonic PPAR gamma expression and gene polymorphisms in patients with Crohn's disease (CD) and ulcerative colitis (UC).

Main Results:

  • TLR4 signaling elevated PPAR gamma expression in a NF-kappa B-dependent manner.
  • Intestinal flora induced PPAR gamma expression in colonic epithelial cells of control mice.
  • UC patients showed significantly reduced colonic PPAR gamma expression compared to controls and CD patients, without gene mutations.

Conclusions:

  • Commensal intestinal flora significantly impacts PPAR gamma expression.
  • PPAR gamma expression is notably impaired in the colonic epithelial cells of ulcerative colitis patients.

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