ArticleBlood advances2020
Neutrophils from hereditary hemochromatosis patients are protected from iron excess and are primed.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Ferroptosis in major depressive disorder: Molecular mechanisms, cellular vulnerability, and therapeutic opportunities.Biochemistry and biophysics reports · 2026Review
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- Cell-Type-Specific Regulation of Ferroptosis in Atherosclerosis: Mechanisms and Therapeutic Potential of Natural Products.Cell biochemistry and function · 2026Review
- Genetic regulation of AIF1 shapes immune and liver injury profiles in chronic alcohol use.JCI insight · 2026Article
- The crosstalk between iron metabolism and immune tolerance in autoimmunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- GATA2 deficiency exacerbates chronic liver injuryWorld journal of stem cells · 2026Article
- Functional alterations of neutrophils from β-thalassemia patients exposed to Pythium insidiosum: An ex vivo study.PloS one · 2026Article
- Iron and the immune system.Nature reviews. Immunology · 2025Review
- Essential role of hepcidin in host resistance to disseminated candidiasis.Cell reports · 2025Article
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Functional consequence of Iron dyshomeostasis and ferroptosis in systemic lupus erythematosus and lupus nephritis.Clinical immunology (Orlando, Fla.) · 2024Review
- A closer look at the role of iron in glioblastoma.Neuro-oncology · 2023Review
- Human red blood cells release microvesicles with distinct sizes and protein composition that alter neutrophil phagocytosis.Journal of extracellular biology · 2023Article
- Circulating neutrophil anti-pathogen dysfunction in cirrhosis.JHEP reports : innovation in hepatology · 2023Review
- Transferrin receptor 2 deficiency promotes macrophage polarization and inflammatory arthritis.Redox biology · 2023Article
- Severe anaemia, iron deficiency, and susceptibility to invasive bacterial infections.Wellcome open research · 2023Review
- Hepcidin and ferritin levels as markers of immune cell activation during septic shock, severe COVID-19 and sterile inflammation.Frontiers in immunology · 2023Article
- Plasma iron controls neutrophil production and function.Science advances · 2022Article
- Iron regulatory protein (IRP)-mediated iron homeostasis is critical for neutrophil development and differentiation in the bone marrow.Science advances · 2022Article
- Isn't it ironic: better RBCs by blocking iron.Blood · 2022Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron is required for the oxidative response of neutrophils to allow the production of reactive oxygen species (ROS). However, neutrophil function may be severely altered in conditions of iron overload, as observed in chronically transfused patients. Therefore, a tight regulation of neutrophil iron homeostasis seems to be critical for avoiding iron toxicity. Hepcidin is the key iron regulator in organisms; however, no studies have investigated its role in maintaining neutrophil iron homeostasis or characterized neutrophil function in patients with hereditary hemochromatosis (HH), a common iron overload genetic disorder that results from a defect in hepcidin production. To explore these issues, we studied 2 mouse models of iron overload: an experimentally induced iron overload model (EIO), in which hepcidin is increased, and a genetic HH model of iron overload with a deletion of hepatic hepcidin. We found that iron-dependent increase of hepatic hepcidin results in neutrophil intracellular iron trapping and consecutive defects in oxidative burst activity. In contrast, in both HH mouse models and HH patients, the lack of hepcidin expression protects neutrophils from toxic iron accumulation. Moreover, systemic iron overload correlated with a surprising neutrophil priming and resulted in a more powerful oxidative burst. Indeed, important factors in neutrophil priming and activation, such as tumor necrosis factor α (TNF-α), VCAM-1, and ICAM-1 are increased in the plasma of HH patients and are associated with an increase in HH neutrophil phagocytosis capacity and a decrease in L-selectin surface expression. This is the first study to characterize neutrophil iron homeostasis and associated functions in patients with HH.
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