Increased deposition of C3b on red cells with low CR1 and CD55 in a malaria-endemic region of western Kenya: Implications for the development of severe anemia

Odhiambo, Collins; Otieno, Walter; Adhiambo, Christine; Odera, Michael M.; Stoute, José A.

doi:10.1186/1741-7015-6-23

Cited by 49 publications

(50 citation statements)

References 34 publications

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“…Studies conducted in areas of P. falciparum endemicity have documented that higher levels of CR1 and CD55 are exhibited in RBCs from children with uncomplicated malaria or who are uninfected than in RBCs from those with severe anemia (119)(120)(121). Furthermore, a study conducted on susceptible children in western Kenya demonstrated an association between low levels of complement regulatory proteins on RBC surfaces and increased risk of C3 deposition on their membranes (125). These data suggest that lower expression levels of such biomarkers would contribute to an increased clearance of erythrocytes, leading to anemia in falciparum malaria.…”

Section: The Complement System and Malariamentioning

confidence: 99%

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

et al. 2014

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The pathogenesis of malaria is complex, generating a broad spectrum of clinical manifestations. One of the major complications and concerns in malaria is anemia, which is responsible for considerable morbidity in the developing world, especially in children and pregnant women. Despite its enormous health importance, the immunological mechanisms involved in malaria-induced anemia remain incompletely understood. Plasmodium vivax, one of the causative agents of human malaria, is known to induce a strong inflammatory response with a robust production of immune effectors, including cytokines and antibodies. Therefore, it is possible that the extent of the immune response not only may facilitate the parasite killing but also may provoke severe illness, including anemia. In this review, we consider potential immune effectors and their possible involvement in generating this clinical outcome during P. vivax infections.

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Section: The Complement System and Malariamentioning

confidence: 99%

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

et al. 2014

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“…The current findings on the functional consequence of RBC CR1 ligation in the immune-transfer process are important especially now when unexpected and non-redundant roles for human RBC CR1 in pathologies ranging from malaria (45) and sepsis (46) to Alzheimer disease (35,(47)(48)(49) are beginning to be unraveled.…”

Section: Discussionmentioning

confidence: 99%

CR1-mediated ATP Release by Human Red Blood Cells Promotes CR1 Clustering and Modulates the Immune Transfer Process

Melhorn¹,

Brodsky²,

Estanislau³

et al. 2013

Journal of Biological Chemistry

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“…Data derived from naturally infected individuals also indicate that after parasite clearance the erythrocyte life span is reduced in patients recovering from P. falciparum or P. vivax malaria (57,58). Hypotheses put forth for the destruction of uninfected erythrocytes have focused on different possible mechanisms including reduced erythrocyte deformability (59,60), accelerated erythrocyte senescence (61), and immunologic removal (62)(63)(64)(65)(66), although none have been conclusively proven to be the mechanism.…”

Section: Fig 11mentioning

confidence: 99%

Plasmodium coatneyi in Rhesus Macaques Replicates the Multisystemic Dysfunction of Severe Malaria in Humans

et al. 2013

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f Severe malaria, a leading cause of mortality among children and nonimmune adults, is a multisystemic disorder characterized by complex clinical syndromes that are mechanistically poorly understood. The interplay of various parasite and host factors is critical in the pathophysiology of severe malaria. However, knowledge regarding the pathophysiological mechanisms and pathways leading to the multisystemic disorders of severe malaria in humans is limited. Here, we systematically investigate infections with Plasmodium coatneyi, a simian malaria parasite that closely mimics the biological characteristics of P. falciparum, and develop baseline data and protocols for studying erythrocyte turnover and severe malaria in greater depth. We show that rhesus macaques (Macaca mulatta) experimentally infected with P. coatneyi develop anemia, coagulopathy, and renal and metabolic dysfunction. The clinical course of acute infections required suppressive antimalaria chemotherapy, fluid support, and whole-blood transfusion, mimicking the standard of care for the management of severe malaria cases in humans. Subsequent infections in the same animals progressed with a mild illness in comparison, suggesting that immunity played a role in reducing the severity of the disease. Our results demonstrate that P. coatneyi infection in rhesus macaques can serve as a highly relevant model to investigate the physiological pathways and molecular mechanisms of malaria pathogenesis in naïve and immune individuals. Together with high-throughput postgenomic technologies, such investigations hold promise for the identification of new clinical interventions and adjunctive therapies.

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Increased deposition of C3b on red cells with low CR1 and CD55 in a malaria-endemic region of western Kenya: Implications for the development of severe anemia

Cited by 49 publications

References 34 publications

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

Potential Immune Mechanisms Associated with Anemia in Plasmodium vivax Malaria: a Puzzling Question

CR1-mediated ATP Release by Human Red Blood Cells Promotes CR1 Clustering and Modulates the Immune Transfer Process

Plasmodium coatneyi in Rhesus Macaques Replicates the Multisystemic Dysfunction of Severe Malaria in Humans

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