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Published on: September 12, 2016
The effects of iron deficiency on neutrophil/monocyte apoptosis in children
S G Berrak1, M Angaji, E Turkkan
1Pediatric Hematology Oncology, Marmara Medical Faculty, Altunizade, Istanbul, Turkey. sberrak@yahoo.com
Insights
Iron deficiency anemia (IDA) impairs phagocytic cell apoptosis, but this is reversible with iron supplementation. This suggests IDA affects immune cell function, with severe cases showing a more pronounced impact.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Iron is vital for DNA synthesis.
- Iron deficiency anemia (IDA) can disrupt cellular processes, including apoptosis.
- Phagocytic cells play a key role in immune responses and clearance of cellular debris.
Purpose of the Study:
- To investigate the effect of IDA on the apoptotic response of phagocytic cells (neutrophils and monocytes).
- To determine if the observed effects of IDA on apoptosis are reversible after iron supplementation.
Main Methods:
- Compared neutrophil and monocyte apoptosis in 49 children with IDA and 26 healthy controls using flow cytometry.
- Administered oral iron supplementation to IDA patients.
- Re-evaluated apoptosis in IDA patients after 15 days of iron therapy and compared to controls.
Main Results:
- IDA patients showed significantly reduced neutrophil and monocyte apoptosis compared to controls.
- Apoptotic responses in IDA patients returned to control levels after 15 days of iron therapy.
- Severe IDA cases exhibited a more pronounced reduction in apoptotic responses than mild IDA cases.
Conclusions:
- IDA can alter neutrophil and monocyte apoptotic responses.
- Iron supplementation therapy can reverse these changes, indicating IDA as a potential cause.
- Further longitudinal studies are needed to assess the long-term impact of IDA on autoimmunity and malignancy.
Objectives:
Iron is essential for DNA synthesis; its deficiency may lead to impaired DNA synthesis and subsequent alterations in levels of apoptosis. Here, we have aimed to investigate effects of iron deficiency anaemia (IDA) on apoptotic response of phagocytic cells and to understand whether the effect is reversible after iron supplementation.
Materials And Methods:
Forty-nine IDA patients and 26 healthy controls, aged between 6 months and 12 years with similar demographic status, were considered. Neutrophil- and monocyte-apoptotic responses of IDA patients and the control group were compared by flow cytometry. Then, IDA patients were provided with oral iron supplementation. On day 15 of iron therapy, neutrophil- and monocyte-apoptotic responses of IDA patients were rechecked and were compared to those of control group.
Results:
Neutrophil- and monocyte-apoptotic responses in terms of early and late percentages of apoptosis, and percentages of necrotic cells, were significantly less in IDA patients compared to the control group. The significantly low apoptotic responses of IDA patients rose to levels of the control group by day 15 of iron therapy. Besides, the effect of IDA on apoptotic responses was found to be more enhanced in severe IDA patients that those of mild IDA patients.
Conclusion:
Correction of differences after iron supplementation therapy implies that IDA might be a cause for changes in neutophil- and monocyte-apoptotic responses. The impact of this diminution of apoptotic cellular function in IDA should be further investigated, with longitudinal studies, in order to document the impact of any severe and/or long-lasting IDA on autoimmunity and malignancy.
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