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Regulation of phagosomal iron release from murine macrophages by nitric oxide
Victoriano Mulero1, Xiao-qing Wei, Foo Y Liew
1Department of Immunology and Bacteriology, Western Infirmary, University of Glasgow, Glasgow, UK. vmulero@um.es
Abstract:
The role of NO in macrophage iron turnover was studied in macrophages from inducible nitric oxide synthase (iNOS)-deficient mice. Interferon gamma/lipopolysaccharide (IFNgamma/LPS)-activated bone marrow-derived macrophages from iNOS-deficient mice, following phagocytosis of 59Fe-labelled transferrin-anti-transferrin immune complexes, showed reduced iron release compared with cells from wild-type iNOS littermates. Uptake of the complexes by macrophages was similar in iNOS-deficient and wild-type mice. Ferritin was up-regulated by IFNgamma/LPS treatment, but NO exercised a modest opposing down-regulatory effect. No effect of iNOS deficiency was seen when iron was taken up from iron citrate, which enters via a non-phagocytic route. These results suggest that NO plays a key role in regulating iron turnover in macrophages acquiring iron by phagocytosis of erythrocytes or cell debris, and thus the supply to peripheral tissues, such as to the bone marrow for erythropoiesis.
Insights
Nitric oxide (NO) is crucial for macrophage iron release, particularly when iron is acquired via phagocytosis. This finding impacts understanding of iron supply to tissues like the bone marrow.
Area of Science:
- Immunology
- Cell Biology
- Hematology
Background:
- Macrophage iron turnover is vital for systemic iron homeostasis.
- Nitric oxide (NO) is implicated in various cellular processes, but its role in macrophage iron metabolism is not fully understood.
Purpose of the Study:
- To investigate the role of inducible nitric oxide synthase (iNOS) in regulating macrophage iron turnover.
- To determine if NO influences iron release from macrophages following phagocytosis.
Main Methods:
- Utilized bone marrow-derived macrophages from iNOS-deficient and wild-type mice.
- Macrophages were activated with interferon-gamma/lipopolysaccharide (IFNγ/LPS).
- Iron uptake and release were assessed using 59Fe-labeled transferrin-anti-transferrin immune complexes and iron citrate.
Main Results:
- iNOS-deficient macrophages exhibited reduced iron release after phagocytosing 59Fe-labeled immune complexes compared to wild-type.
- Iron uptake was comparable between iNOS-deficient and wild-type macrophages.
- IFNγ/LPS upregulated ferritin, while NO showed a modest opposing effect.
- No difference in iron uptake from iron citrate was observed, indicating a phagocytosis-dependent mechanism.
Conclusions:
- NO produced by iNOS plays a significant role in regulating iron release from macrophages that acquire iron via phagocytosis.
- This NO-mediated regulation impacts iron supply to peripheral tissues, including the bone marrow for erythropoiesis.
- Findings highlight NO as a key regulator of macrophage iron metabolism in specific iron acquisition pathways.
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