Immune-protective effect of echinococcosis on colitis experimental model is dependent of down regulation of TNF-α and NO production

Acta Trop. 2017 Feb;166:7-15. doi: 10.1016/j.actatropica.2016.10.020. Epub 2016 Oct 27.

Abstract

Hydatid disease (echinococcosis) is a chronic, endemic helminthic disease caused by the larval stage of the tapeworm, Echinococcus granulosus. This disease is endemic in many parts of the world, such as the Mediterranean area, and in particular in Algeria. Helminth parasites have developed complex strategies to modulate the immune responses of their hosts through versatile immune-regulatory mechanisms. These mechanisms may regulate immune responses associated with inflammatory diseases such as inflammatory bowel diseases (IBD). the goal of this study was to investigate the effect of Echinococcus granulosus infection on the development of dextran sulfate sodium (DSS)-induced colitis. Our results demonstrated that E. granulosus infection significantly improved the clinical symptoms and histological scores observed during DSS-induced colitis, and also maintained mucus production by goblet cells. Interestingly, this infection reduced Nitric oxide (NO) and tumor necrosis factor α (TNF-α) production and attenuated inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NF-κB) expression in colonic tissues. Collectively, our data support the hygiene hypothesis and indicate that prior infection with E. granulosus can effectively protect mice from DSS-induced colitis by enhancing immune-regulatory mechanisms.

Keywords: Echinococcus granulosus; Experimental colitis; Helminth; Inflammatory bowel disease (IBD); Nitric oxide (NO); Tumor necrosis factor (TNF)-α.

MeSH terms

  • Algeria
  • Animals
  • Colitis / chemically induced
  • Colitis / complications
  • Colitis / immunology*
  • Dextran Sulfate
  • Disease Models, Animal
  • Down-Regulation
  • Echinococcosis / complications*
  • Female
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type II / metabolism
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Dextran Sulfate
  • Nitric Oxide Synthase Type II