Role of the complement system in the pathogenesis of severe malaria - an in vitro model approach
Malaria; Plasmodium falciparum; Complement System
Malaria is a parasitic infectious disease, caused by protozoa of the genus Plasmodium and characterized by acute fever, chills, sweating, and headache. Six species cause human malaria in the world: P. falciparum, P. vivax, P. malariae, P. ovale and P. knowlesi and P. simium. Most cases of severe malaria human infection are attributed to infections by Plasmodium falciparum, considered the most aggressive due to tissue hypoxia resulting from several factors, including severe anemia. According to the 2017 World Malaria Report, there were about 219 million cases of malaria and 435,000 deaths from the disease each year. As an intracellular parasite, Plasmodium depends on the host to survive and genetically determined factors can influence the individual's susceptibility to clinically developing malaria, especially those that result in abnormalities hematological. Thus, the present study aims to evaluate the participation of the complement system in the genesis of the phenomenon of hemolysis induced by P. falciparum in vitro models and in the second moment, to develop and standardize in vitro methodologies for understanding the mechanism of hemolysis of human erythrocytes treated with P. falciparum total proteins mediated by the complement system. For this, the methodology includes the in vitro cultivation of the W2 strain of P. falciparum, in addition to animal experimentation using Swiss mice immunized with protein extract from the culture of P. falciparum for the production of polyclonal serum, in addition to autologous hemolytic assays and determination of complement fragments by flow cytometry.