Inflammation and Chagas disease some mechanisms and relevance

Adv Parasitol. 2011:76:171-94. doi: 10.1016/B978-0-12-385895-5.00008-6.

Abstract

Chagas cardiomyopathy is caused by infection with flagellated protozoan Trypanosoma cruzi. In patients, there is a fine balance between control of the replication and the intensity of the inflammatory response so that the host is unable to eliminate the parasite resulting in the parasite persisting as a lifelong infection in most individuals. However, the parasite persists in such a way that it causes no or little disease. This chapter reviews our understanding of many of the mediators of inflammation and cells which are involved in the inflammatory response of mammals to T. cruzi infection. Particular emphasis is given to the role of chemokines, endothelin and lipid mediators. Understanding the full range of mediators and cells present and how they interact with each other in Chagas disease may shed light on how we modulate disease pathogenesis and define new approaches to treat or prevent the disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Chagas Cardiomyopathy / immunology*
  • Chagas Cardiomyopathy / pathology*
  • Chemokines / metabolism
  • Eicosanoids / metabolism
  • Endothelins / metabolism
  • Host-Pathogen Interactions*
  • Humans
  • Inflammation / immunology*
  • Inflammation / parasitology
  • Inflammation / pathology*
  • Inflammation Mediators / metabolism
  • Mammals
  • Trypanosoma cruzi / immunology*
  • Trypanosoma cruzi / pathogenicity*

Substances

  • Chemokines
  • Eicosanoids
  • Endothelins
  • Inflammation Mediators