Cytoadherence, pathogenesis and the infected red cell surface in Plasmodium falciparum

Newbold, Chris; Craig, Alister G.; Kyes, Sue; Rowe, J. Alexandra; Fernández-Reyes, Delmiro; Fagan, Toby

doi:10.1016/s0020-7519(99)00049-1

Cited by 142 publications

(105 citation statements)

References 57 publications

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“…Sequestration in peripheral sites such as skin might be expected to facilitate transmission (58) while at the same time not compromise host survival. This hypothesis is supported by the work of Newbold and colleagues, who have reported that significantly higher binding to CD36 occurs in cases of nonsevere disease (25). More recent population data has linked CD36 deficiency with an increased susceptibility to severe and cerebral malaria (27).…”

Section: Figurementioning

confidence: 75%

“…CD36 is primarily expressed by monocytes, M s, adipocytes, myocytes, and endothelial cells of the skin and reticuloendothelial system, especially the liver and spleen (5). Increased sequestration in these sites would not be expected to directly contribute to excess mortality, because binding within the reticuloendothelial system should theoretically enhance clearance, and binding to CD36 in nonvital sites has been proposed to confer protection against severe and cerebral disease (25,27,42). However, it will be important to determine whether these agents up-regulate CD36 in microvascular endothelium of vital organs such as the brain.…”

Section: Figurementioning

confidence: 99%

“…The identification of CD36 as a major sequestration receptor has led to the assumption that it contributes to the pathophysiology of severe malaria and has prompted the development of antiadherence therapies to disrupt the CD36-PE interaction (7,18,(22)(23). However, its role in cerebral and severe malaria is unclear because little CD36 is expressed on cerebral microvasculature endothelial cells (5,24), and studies have reported that significantly higher binding of PEs to CD36 occurs in cases of nonsevere malaria (25,26). Furthermore, individuals deficient in CD36 were found to be more susceptible to severe and cerebral malaria (27).…”

mentioning

confidence: 99%

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Peroxisome Proliferator-Activated Receptor γ-Retinoid X Receptor Agonists Increase CD36-Dependent Phagocytosis ofPlasmodium falciparum-Parasitized Erythrocytes and Decrease Malaria-Induced TNF-α Secretion by Monocytes/Macrophages

Serghides

Kain

2001

The Journal of Immunology

101

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Severe and fatal malaria is associated with the failure of host defenses to control parasite replication, excessive secretion of proinflammatory cytokines such as TNF-α, and sequestration of parasitized erythrocytes (PEs) in vital organs. The identification of CD36 as a major sequestration receptor has led to the assumption that it contributes to the pathophysiology of severe malaria and has prompted the development of antiadherence therapies to disrupt the CD36-PE interaction. This concept has been challenged by unexpected evidence that individuals deficient in CD36 are more susceptible to severe and cerebral malaria. In this study, we demonstrate that CD36 is the major receptor mediating nonopsonic phagocytosis of PEs by macrophages, a clearance mechanism of potential importance in nonimmune hosts at the greatest risk of severe malaria. CD36-mediated uptake of PEs occurs via a novel pathway that does not involve thrombospondin, the vitronectin receptor, or phosphatidylserine recognition. Furthermore, we show that proliferator-activated receptor γ-retinoid X receptor agonists induce an increase in CD36-mediated phagocytosis and a decrease in parasite-induced TNF-α secretion. Specific up-regulation of monocyte/macrophage CD36 may represent a novel therapeutic strategy to prevent or treat severe malaria.

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Section: Figurementioning

confidence: 75%

Section: Figurementioning

confidence: 99%

mentioning

confidence: 99%

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Peroxisome Proliferator-Activated Receptor γ-Retinoid X Receptor Agonists Increase CD36-Dependent Phagocytosis ofPlasmodium falciparum-Parasitized Erythrocytes and Decrease Malaria-Induced TNF-α Secretion by Monocytes/Macrophages

Serghides

Kain

2001

The Journal of Immunology

101

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“…P. falciparum, during development inside RBC induces formation of sticky knobs on the surface of the erythrocytes. 45 These knobs bind to receptors on endothelial cells in capillaries and venules. Infected red cells also stick to uninfected red cells and form rosettes which clog the microcirculation.…”

Section: Malarial Hepatopathymentioning

confidence: 99%

Approach to Clinical Syndrome of Jaundice and Encephalopathy in Tropics

Anand

Garg

2015

Journal of Clinical and Experimental Hepatology

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“…Thus, this process gives rise to functional cellular hypoxia rather than simply the effects of the vaso-occlusive phenomenon. [13][14][15] Diagnosis Malaria usually presents as an acute febrile illness ten to 15 days after inoculation with non-specific symptoms of Adapted from WHO guidelines for the treatment of malaria 22 Perioperative considerations of malaria 307…”

Section: Plasmodium Life Cyclementioning

confidence: 99%

Perioperative considerations of the patient with malaria

Soltanifar

Carvalho

Sultan

2014

Can J Anesth/J Can Anesth

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Purpose Malaria is a life-threatening infectious disease caused by the Plasmodium parasite. Increased global travel has resulted in an escalation in the number of imported cases seen in developed countries. Patients with malaria may present for surgery in both endemic and nonendemic countries. This article reviews the perioperative considerations when managing patients with malaria. Source A literature review of anesthesia, perioperative care, and malaria-related articles was performed using the MEDLINE Ò , EMBASE TM , and Web of Science databases to identify relevant articles published in English during . Of the 303 articles matching the search criteria, 265 were excluded based on title and abstract. Eleven of the remaining 38 articles were relevant to anesthesia/perioperative care, and 27 articles were identified as having direct relevance to critical care medicine. Principal findings The majority of imported malaria cases are caused by the falciparum species, which is associated with the greatest degree of morbidity and mortality. Various organ systems may be impacted as a consequence of changes in the structure and function of parasitized erythrocytes. Preoperative assessment should focus on establishing the species of malaria, the severity of disease, assessing the degree of end-organ impairment, and initiating treatment of malaria prior to surgery. Intravenous artesunate is the treatment of choice for severe falciparum malaria. Quinine is a second-line agent but has a narrow therapeutic index and particularly hazardous side effects. Intraoperatively, attention should focus on fluid management, dynamics of cerebral blood flow, and avoidance of hypoglycemia. Postoperative care of severe cases should ideally take place in a critical care unit as there may be ongoing requirements for multi-organ support, including renal replacement therapy, ventilation, and/or inotropic support. The safety of neuraxial anesthesia has not been well studied in the setting of malaria. Conclusions Malaria remains one of the most devastating infectious diseases worldwide. Multiple organ systems can be impacted as a consequence of changes in structure and function of parasitized erythrocytes. Safe perioperative management requires a sound knowledge of all these potential system effects. RésuméObjectif Le paludisme est une maladie infectieuse possiblement fatale due au parasite Plasmodium. La multiplication des voyages à travers le monde a entraîné un accroissement du nombre de cas importés observés dans les pays développés. Les patients atteints de paludisme peuvent nécessiter une chirurgie, aussi bien dans les pays où la maladie est endémique que dans les autres. Cet article passe en revue les considérations périopératoires lors de la prise en charge de patients atteints de paludisme. Source Une revue de la littérature à la recherche d'articles d'anesthésie, de soins périopératoires et en Author contributions Daniel Soltanifar, Brendan Carvalho, and Pervez Sultan all made substantial contributions to the literature review, ...

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Cytoadherence, pathogenesis and the infected red cell surface in Plasmodium falciparum

Cited by 142 publications

References 57 publications

Peroxisome Proliferator-Activated Receptor γ-Retinoid X Receptor Agonists Increase CD36-Dependent Phagocytosis ofPlasmodium falciparum-Parasitized Erythrocytes and Decrease Malaria-Induced TNF-α Secretion by Monocytes/Macrophages

Peroxisome Proliferator-Activated Receptor γ-Retinoid X Receptor Agonists Increase CD36-Dependent Phagocytosis ofPlasmodium falciparum-Parasitized Erythrocytes and Decrease Malaria-Induced TNF-α Secretion by Monocytes/Macrophages

Approach to Clinical Syndrome of Jaundice and Encephalopathy in Tropics

Perioperative considerations of the patient with malaria

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