Differences in iNOS and arginase expression and activity in the macrophages of rats are responsible for the resistance against T. gondii infection

PLoS One. 2012;7(4):e35834. doi: 10.1371/journal.pone.0035834. Epub 2012 Apr 25.

Abstract

Toxoplasma gondii infects humans and warm blooded animals causing devastating disease worldwide. It has long been a mystery as to why the peritoneal macrophages of rats are naturally resistant to T. gondii infection while those of mice are not. Here, we report that high expression levels and activity of inducible nitric oxide synthase (iNOS) and low levels of arginase-1 (Arg 1) activity in the peritoneal macrophages of rats are responsible for their resistance against T. gondii infection, due to high nitric oxide and low polyamines within these cells. The opposite situation was observed in the peritoneal macrophages of mice. This discovery of the opposing functions of iNOS and Arg 1 in rodent peritoneal macrophages may lead to a better understanding of the resistance mechanisms of mammals, particularly humans and livestock, against T. gondii and other intracellular pathogens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arginase / genetics*
  • Arginase / metabolism
  • Disease Resistance / physiology*
  • Gene Expression
  • Host Specificity
  • Humans
  • Macrophage Activation
  • Macrophages, Peritoneal / enzymology*
  • Macrophages, Peritoneal / immunology
  • Macrophages, Peritoneal / parasitology
  • Mice
  • Mice, Inbred Strains
  • Nitric Oxide / biosynthesis
  • Nitric Oxide Synthase Type II / genetics*
  • Nitric Oxide Synthase Type II / metabolism
  • Rats
  • Rats, Inbred Strains
  • Rodent Diseases*
  • Toxoplasma / physiology
  • Toxoplasmosis, Animal / enzymology*
  • Toxoplasmosis, Animal / immunology
  • Toxoplasmosis, Animal / parasitology

Substances

  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Arginase