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cytoadherence

Not Open Access | Complement C1s cleaves PfEMP1 at interdomain conserved sites inhibiting Plasmodium falciparum cytoadherence

June 1, 2021 - 12:26 -- NOT Open Access
Author(s): 
Azasi Y, Low LM, Miller LH, et al.
Reference: 
Proc Natl Acad Sci U S A. 2021 Jun 1;118(22):e2104166118

Cytoadhesion of Plasmodium falciparum-infected erythrocytes (IEs) to the endothelial lining of blood vessels protects parasites from splenic destruction, but also leads to detrimental inflammation and vessel occlusion. Surface display of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) adhesion ligands exposes them to host antibodies and serum proteins. PfEMP1 are important targets of acquired immunity to malaria, and through evolution, the protein family has expanded and diversified to bind a select set of host receptors through antigenically diversified receptor-binding domains.

NOT Open Access | Hemozoin is a potential threat in cerebral malaria pathology through the induction of RBC-EC cytoadherence

February 23, 2021 - 13:18 -- NOT Open Access
Author(s): 
Mehra A, Balaji SN, Trivedi V
Reference: 
Acta Trop. 2021 Feb 18:105867

Cerebral malaria is an outcome of multifaceted and complicated condition. Cytoadherence is one critical factor in cerebral malaria pathology as high order cytoadherence complexes result in vascular congestion and cell apoptosis. Morphological abnormalities in uninfected RBCs can be a contributing factor to aggravate cytoadherence. Malaria pigment hemozoin is a potential bioactive molecule and the role of this pigment in cerebral malaria pathology is not completely understood. To understand this, primarily we investigated the impact of hemozoin pigment on uninfected RBCs.

Plasma-derived extracellular vesicles from Plasmodium vivax patients signal spleen fibroblasts via NF-kB facilitating parasite cytoadherence

June 3, 2020 - 15:52 -- Open Access
Author(s): 
Toda H, Diaz-Varela M, Del Portillo HA, et al.
Reference: 
Nat Commun. 2020 Jun 2; 11(1):2761

Plasmodium vivax is the most widely distributed human malaria parasite. Previous studies have shown that circulating microparticles during P. vivax acute attacks are indirectly associated with severity. Extracellular vesicles (EVs) are therefore major components of circulating plasma holding insights into pathological processes. Here, we demonstrate that plasma-derived EVs from Plasmodium vivax patients (PvEVs) are preferentially uptaken by human spleen fibroblasts (hSFs) as compared to the uptake of EVs from healthy individuals.

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