Infection with a helminth parasite prevents experimental colitis via a macrophage-mediated mechanism

J Immunol. 2007 Apr 1;178(7):4557-66. doi: 10.4049/jimmunol.178.7.4557.


The propensity of a range of parasitic helminths to stimulate a Th2 or regulatory cell-biased response has been proposed to reduce the severity of experimental inflammatory bowel disease. We examined whether infection with Schistosoma mansoni, a trematode parasite, altered the susceptibility of mice to colitis induced by dextran sodium sulfate (DSS). Mice infected with schistosome worms were refractory to DSS-induced colitis. Egg-laying schistosome infections or injection of eggs did not render mice resistant to colitis induced by DSS. Schistosome worm infections prevent colitis by a novel mechanism dependent on macrophages, and not by simple modulation of Th2 responses, or via induction of regulatory CD4+ or CD25+ cells, IL-10, or TGF-beta. Infected mice had marked infiltration of macrophages (F4/80+CD11b+CD11c(-)) into the colon lamina propria and protection from DSS-induced colitis was shown to be macrophage dependent. Resistance from colitis was not due to alternatively activated macrophages. Transfer of colon lamina propria F4/80+ macrophages isolated from worm-infected mice induced significant protection from colitis in recipient mice treated with DSS. Therefore, we propose a new mechanism whereby a parasitic worm suppresses DSS-induced colitis via a novel colon-infiltrating macrophage population.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / immunology*
  • Dextran Sulfate / toxicity
  • Immune Tolerance*
  • Interleukin-10 / metabolism
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred Strains
  • Models, Animal
  • Mucous Membrane / immunology
  • Ovum / immunology
  • Schistosoma mansoni*
  • Schistosomiasis mansoni / immunology*
  • T-Lymphocytes, Regulatory / immunology
  • Th2 Cells / immunology
  • Transforming Growth Factor beta / metabolism


  • Transforming Growth Factor beta
  • Interleukin-10
  • Dextran Sulfate