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The C5a receptor antagonist PMX205 ameliorates experimentally induced colitis associated with increased IL-4 and

U Jain1, T M Woodruff, A W Stadnyk

  • 1Department of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.

British Journal of Pharmacology
|August 29, 2012
PubMed
Abstract

Insights

PMX205, a C5a receptor antagonist, effectively reduced inflammation in a mouse model of inflammatory bowel disease (IBD). This study supports targeting the C5a receptor (CD88) as a potential therapy for IBD patients.

Area of Science:

  • Immunology
  • Gastroenterology
  • Pharmacology

Background:

  • Inflammatory bowel diseases (IBD) lack effective anti-complement therapies.
  • Blocking C5a shows promise in rodent colitis models.
  • The C5a receptor (CD88) is a potential therapeutic target.

Purpose of the Study:

  • To evaluate the efficacy, mechanism, and specificity of PMX205, an oral C5a receptor antagonist.
  • To investigate PMX205 in the dextran sulphate sodium (DSS) model of murine colitis.

Main Methods:

  • Mice received oral PMX205 (100 or 200 μg/day) in prophylactic and therapeutic settings.
  • Assessed clinical illness, colon histology, and inflammatory mediator generation.
  • Tested PMX205 in different mouse strains and in CD88-deficient mice.

Main Results:

  • PMX205 significantly prevented DSS-induced colon inflammation.
  • Reduced pro-inflammatory cytokines and nitrotyrosine staining.
  • Increased anti-inflammatory cytokines (IL-4, IL-10); inactive in CD88-deficient mice.

Conclusions:

  • PMX205 is efficacious in preventing DSS-induced colitis.
  • Targeting CD88 with PMX205 is a potential therapeutic strategy for IBD.

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