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

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Article numbere82874
JournalPLoS One
Volume8
Issue number12
DOIs
Publication statusPublished - Dec 9 2013

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

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