ArticleAmerican journal of hematology2011
Mechanisms of erythropoiesis inhibition by malarial pigment and malaria-induced proinflammatory mediators in an in vitro model.
Article in American journal of hematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Reduced systemic bicyclo-prostaglandin-E2 and cyclooxygenase-2 gene expression are associated with inefficient erythropoiesis and enhanced uptake of monocytic hemozoin in children with severe malarial anemia.American journal of hematology · 2012Trial
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- FRRS1L variants and ferriheme overload drive hyperpigmentation and systemic Iron overload in lanping black bone sheep.Cell & bioscience · 2025Article
- Impact of age, HIV1, sickle-cell genotypes, and interferon-gamma gene upstream variants on malaria disease outcomes in a longitudinal pediatric cohort.Scientific reports · 2025Article
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- Transcriptomic and Proteomic Insights into Host Immune Responses in Pediatric Severe Malarial Anemia: Dysregulation in HSP60-70-TLR2/4 Signaling and Altered Glutamine Metabolism.Pathogens (Basel, Switzerland) · 2024Article
- Entire expressed peripheral blood transcriptome in pediatric severe malarial anemia.Nature communications · 2024Article
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- Erythropoiesis and Malaria, a Multifaceted Interplay.International journal of molecular sciences · 2022Review
- Implication of asymptomatic and clinical Plasmodium falciparum infections on biomarkers of iron status among school-aged children in Malawi.Malaria journal · 2022Article
- Deferiprone-Resveratrol Hybrid, an Iron-Chelating Compound, Acts as an Antimalarial and Hepatoprotective Agent inBioinorganic chemistry and applications · 2022Article
- Nonsynonymous amino acid changes in the α-chain of complement component 5 influence longitudinal susceptibility toFrontiers in genetics · 2022Article
- The Potential Role ofJournal of tropical medicine · 2021Article
- A primate model of severe malarial anaemia: a comparative pathogenesis study.Scientific reports · 2019Article
- Molecular basis of reduced LAIR1 expression in childhood severe malarial anaemia: Implications for leukocyte inhibitory signalling.EBioMedicine · 2019Article
- Hematologic changes and splenic index on malaria mice models givenVeterinary world · 2019Article
- Molecular Principles of Intrauterine Growth Restriction in Plasmodium Falciparum Infection.Frontiers in endocrinology · 2019Review
- A novel in vitro model reveals distinctive modulatory roles of Plasmodium falciparum and Plasmodium vivax on naïve cell-mediated immunity.Malaria journal · 2017Article
- Evidencing the Role of Erythrocytic Apoptosis in Malarial Anemia.Frontiers in cellular and infection microbiology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
One of the commonest complications of Plasmodium falciparum malaria is the development of severe malarial anemia (SMA), which is, at least in part, due to malaria-induced suppression of erythropoiesis. Factors associated with suppression of erythropoiesis and development of SMA include accumulation of malarial pigment (hemozoin, PfHz) in bone marrow and altered production of inflammatory mediators, such as tumor necrosis factor (TNF)-α, and nitric oxide (NO). However, studies investigating the specific mechanisms responsible for inhibition of red blood cell development have been hampered by difficulties in obtaining bone marrow aspirates from infants and young children, and the lack of reliable models for examining erythroid development. As such, an in vitro model of erythropoiesis was developed using CD34+ stem cells derived from peripheral blood to examine the effects of PfHz, PfHz-stimulated peripheral blood mononuclear cell (PBMC)-conditioned media (CM-PfHz), TNF-α, and NO on erythroid cell development. PfHz only slightly suppressed erythroid cell proliferation and maturation marked by decreased expression of glycophorin A (GPA). On the other hand, CM-PfHz, TNF-α, and NO significantly inhibited erythroid cell proliferation. Furthermore, decreased proliferation in cells treated with CM-PfHz and NO was accompanied by increased apoptosis of erythropoietin-stimulated CD34+ cells. In addition, NO significantly inhibited erythroid cell maturation, whereas TNF-α did not appear to be detrimental to maturation. Collectively, our results demonstrate that PfHz suppresses erythropoiesis by acting both directly on erythroid cells, and indirectly via inflammatory mediators produced from PfHz-stimulated PBMC, including TNF-α and NO.
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