PLoS ONE (Jan 2013)

Mycobacterium avium infection induces H-ferritin expression in mouse primary macrophages by activating Toll-like receptor 2.

  • Sandro Silva-Gomes,
  • Cécile Bouton,
  • Tânia Silva,
  • Paolo Santambrogio,
  • Pedro Rodrigues,
  • Rui Appelberg,
  • Maria Salomé Gomes

DOI
https://doi.org/10.1371/journal.pone.0082874
Journal volume & issue
Vol. 8, no. 12
p. e82874

Abstract

Read online

Important for both host and pathogen survivals, iron is a key factor in determining the outcome of an infectious process. Iron with-holding, including sequestration inside tissue macrophages, is considered an important strategy to fight infection. However, for intra-macrophagic pathogens, such as Mycobacterium avium, host defence may depend on intracellular iron sequestration mechanisms. Ferritin, the major intracellular iron storage protein, plays a critical role in this process. In the current study, we studied ferritin expression in mouse bone marrow-derived macrophages upon infection with M. avium. We found that H-ferritin is selectively increased in infected macrophages, through an up-regulation of gene transcription. This increase was mediated by the engagement of Toll like receptor-2, and was independent of TNF-alpha or nitric oxide production. The formation of H-rich ferritin proteins and the consequent iron sequestration may be an important part of the panoply of antimicrobial mechanisms of macrophages.