Journal ArticleDOI
Putative pathophysiological interactions of cytokines and phagocytic cells in severe human falciparum malaria
TLDR
The putative mechanisms by which cytokines may mediate both beneficial and deleterious effects by activating phagocytic cells in severe falciparum malaria are discussed.Abstract:
The severe disease and high mortality associated with Plasmodium falciparum infection have traditionally been attributed solely to parasitic virulence factors, but more recent evidence suggests that the host's immunologic response may also contribute to the pathophysiology of the disease in humans. This response would be expected to be proportionate--in intensity and nature--to the antigenic load created by the sequestration of parasites in the microvasculature and to be directed against the sites of maximal parasitization; thus the immunologic response could potentially contribute to the pathophysiology of both survival and fatal outcome in severe infection. Cytokines appear to play a pivotal role in the activation of the immune response in human falciparum malaria, and their levels correlate with disease severity. The putative mechanisms by which cytokines may mediate both beneficial and deleterious effects by activating phagocytic cells in severe falciparum malaria are discussed.read more
Citations
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Serum levels of the proinflammatory cytokines interleukin-1 beta (IL-1β), IL-6, IL-8, IL-10, tumor necrosis factor alpha, and IL-12(p70) in malian children with severe Plasmodium falciparum malaria and matched uncomplicated malaria or healthy controls
Kirsten E. Lyke,R. Burges,Yacouba Cissoko,Lansana Sangaré,M. Dao,Issa Diarra,Abdoulaye K. Kone,R. Harley,Christopher V. Plowe,Ogobara K. Doumbo,Marcelo B. Sztein +10 more
TL;DR: The complex relationships between inflammatory cytokines and disease in P. falciparum malaria among children aged 3 months to 14 years residing in Bandiagara, Mali, are illustrated.
Journal ArticleDOI
Nonopsonic monocyte/macrophage phagocytosis of Plasmodium falciparum-parasitized erythrocytes: a role for CD36 in malarial clearance
TL;DR: CD36-dependent binding and signaling appears to be crucial for the nonopsonic clearance of PEs and does not appear to contribute to the increase in TNF-alpha that is prognostic of poor outcome in clinical malaria.
Journal ArticleDOI
Blood Coagulation, Inflammation, and Malaria
TL;DR: The Tissue Factor Model (TFM) for malaria pathogenesis is presented, which places TF as the interface between sequestration, endothelial cell (EC) activation, blood coagulation disorder, and inflammation often associated with the disease.
Journal ArticleDOI
Malarial acute renal failure.
TL;DR: It was only in 1880 that Charles Laveran, a French physician working in Algeria, discovered the true causative agent as being a sporozoan of the genus Plasmodium, and to map the malaria genome, identifying a huge number of genes located on 14 chromosomes.
Journal ArticleDOI
Hemozoin Induces Macrophage Chemokine Expression through Oxidative Stress-Dependent and -Independent Mechanisms
TL;DR: The molecular mechanisms underlying HZ-inducible macrophage (Mφ) chemokine mRNA expression are investigated to better understand the molecular mechanisms through which parasite components, such as HZ, modulate the immune response during malaria infection.
References
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