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Updated: May 4, 2026
Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
Published on: April 29, 2015
Mycobacterium avium infection induces H-ferritin expression in mouse primary macrophages by activating Toll-like
Sandro Silva-Gomes1, Cécile Bouton2, Tânia Silva1
1IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal ; ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal.
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.
Insights
Host defense against Mycobacterium avium involves iron sequestration by H-ferritin in macrophages. This process, triggered by Toll-like receptor 2, highlights ferritin
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Iron is crucial for host and pathogen survival during infection.
- Iron withholding by macrophages is a key host defense strategy.
- Intracellular pathogens like Mycobacterium avium may be controlled by intracellular iron sequestration.
Purpose of the Study:
- To investigate ferritin expression in mouse macrophages infected with Mycobacterium avium.
- To elucidate the mechanisms regulating ferritin expression during M. avium infection.
Main Methods:
- Analysis of ferritin expression in mouse bone marrow-derived macrophages.
- Assessment of gene transcription for ferritin.
- Investigation of the role of Toll-like receptor-2 (TLR2), TNF-alpha, and nitric oxide in ferritin regulation.
Main Results:
- H-ferritin expression is selectively increased in M. avium-infected macrophages.
- This increase is due to enhanced H-ferritin gene transcription.
- TLR2 engagement mediates H-ferritin upregulation, independent of TNF-alpha or nitric oxide.
Conclusions:
- Upregulation of H-ferritin in macrophages is an important host defense mechanism against M. avium.
- Iron sequestration by H-rich ferritin contributes to macrophage antimicrobial activity.
- TLR2 signaling plays a critical role in initiating this iron-scavenging response.
