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Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
Published on: October 25, 2017
Salmonella acquires ferrous iron from haemophagocytic macrophages
Toni A Nagy1, Sarah M Moreland, Corrella S Detweiler
1Department of Molecular, Cellular and Developmental Biology, University of Colorado-Boulder, Boulder, CO, USA.
Abstract:
Bacteria harbour both ferrous and ferric iron transporters. We now report that infection of macrophages and mice with a Salmonella enterica Typhimurium strain containing an inactivated feoB-encoded ferrous iron transporter results in increased bacterial replication, compared to infection with wild type. Inactivation of other cation transporters, SitABCD or MntH, did not increase bacterial replication. The feoB mutant strain does not have an intrinsically faster growth rate. Instead, increased replication correlated with increased expression in macrophages of the fepB-encoded bacterial ferric iron transporter and also required siderophores, which capture ferric iron. Co-infection of mice with wild type and a feoB mutant strain yielded a different outcome: FeoB is clearly required for tissue colonization. In co-infected primary mouse macrophages, FeoB is required for S. Typhimurium replication if the macrophages were IFNγ treated and contain phagocytosed erythrocytes, a model for haemophagocytosis. Haemophagocytes are macrophages that have engulfed erythrocytes and/or leucocytes and can harbour Salmonella in mice. These observations suggest that Salmonella acquires ferrous iron from haemophagocytic macrophages.
Insights
Salmonella Typhimurium lacking the ferrous iron transporter FeoB shows increased replication in macrophages. FeoB is crucial for Salmonella tissue colonization and iron acquisition from host cells.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Bacteria utilize various iron transporters to scavenge essential iron from host environments.
- Iron availability is a critical factor influencing bacterial growth and virulence during infection.
- Salmonella enterica Typhimurium employs both ferrous and ferric iron uptake systems.
Purpose of the Study:
- To investigate the role of the ferrous iron transporter FeoB in Salmonella Typhimurium infection.
- To determine the impact of FeoB inactivation on bacterial replication and virulence in host cells and animal models.
- To elucidate the mechanisms by which Salmonella acquires iron during macrophage infection.
Main Methods:
- Generating a feoB mutant strain of Salmonella Typhimurium.
- Infecting primary mouse macrophages and live mice with wild-type and mutant strains.
- Assessing bacterial replication rates and tissue colonization.
- Analyzing the expression of iron transporters and the requirement for siderophores.
- Utilizing IFNγ-treated macrophages with phagocytosed erythrocytes to model haemophagocytosis.
Main Results:
- Inactivation of feoB led to increased Salmonella replication within macrophages, unlike mutations in SitABCD or MntH.
- The feoB mutant did not exhibit an intrinsic growth defect.
- Increased replication of the feoB mutant correlated with enhanced expression of the ferric iron transporter fepB and required siderophores.
- FeoB was essential for Salmonella tissue colonization in a co-infection model.
- FeoB-mediated replication was observed in IFNγ-treated macrophages containing phagocytosed erythrocytes, suggesting iron acquisition from haemophagocytes.
Conclusions:
- The ferrous iron transporter FeoB plays a significant role in Salmonella Typhimurium virulence, particularly in tissue colonization.
- FeoB is required for Salmonella replication in specific macrophage environments, such as haemophagocytes, indicating its importance in iron acquisition from these cells.
- Salmonella Typhimurium likely acquires ferrous iron from haemophagocytic macrophages via the FeoB transporter.
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