On the cytoadhesion of Plasmodium vivax-infected erythrocytes
| Autor: | Juliana A. Leite, Hernando A. del Portillo, Patrícia Puccinelli Orlandi, Fabio T. M. Costa, Stefanie C. P. Lopes, Ronei Luciano Mamoni, Tatiane R. Oliveira, Laurent Rénia, Bruna O. Carvalho, Rossarin Suwanarusk, Irene S. Soares, Maria Ophelia G. De Araújo, Daniel Y. Bargieri, Paulo Nogueira, Mauricio M. Rodrigues, Yara C. Blanco, Georges Snounou, Bruce Russell, Gerhard Wunderlich, Marcus V. G. Lacerda |
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| Rok vydání: | 2010 |
| Předmět: |
Erythrocytes
PARASITOLOGIA Placenta Plasmodium vivax Pathogenesis Blood cell Apicomplexa Pregnancy parasitic diseases medicine Cell Adhesion Malaria Vivax Immunology and Allergy Animals Humans Saimiri biology Endothelial Cells Plasmodium falciparum biology.organism_classification medicine.disease Virology Red blood cell Infectious Diseases medicine.anatomical_structure Protozoa Female Malaria |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| ISSN: | 1537-6613 |
| Popis: | Background Plasmodium falciparum and Plasmodium vivax are responsible for most of the global burden of malaria. Although the accentuated pathogenicity of P. falciparum occurs because of sequestration of the mature erythrocytic forms in the microvasculature, this phenomenon has not yet been noted in P. vivax. The increasing number of severe manifestations of P. vivax infections, similar to those observed for severe falciparum malaria, suggests that key pathogenic mechanisms (eg, cytoadherence) might be shared by the 2 parasites. Methods Mature P. vivax-infected erythrocytes (Pv-iEs) were isolated from blood samples collected from 34 infected patients. Pv-iEs enriched on Percoll gradients were used in cytoadhesion assays with human lung endothelial cells, Saimiri brain endothelial cells, and placental cryosections. Results Pv-iEs were able to cytoadhere under static and flow conditions to cells expressing endothelial receptors known to mediate the cytoadhesion of P. falciparum. Although Pv-iE cytoadhesion levels were 10-fold lower than those observed for P. falciparum-infected erythrocytes, the strength of the interaction was similar. Cytoadhesion of Pv-iEs was in part mediated by VIR proteins, encoded by P. vivax variant genes (vir), given that specific antisera inhibited the Pv-iE-endothelial cell interaction. Conclusions These observations prompt a modification of the current paradigms of the pathogenesis of malaria and clear the way to investigate the pathophysiology of P. vivax infections. |
| Databáze: | OpenAIRE |
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