Resistance and Susceptibility to Malarial Infection: A Host De¬fense Strategy against Malaria
BAKIR، Hanaa نويسنده Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt BAKIR, Hanaa , YONES، Doaa نويسنده Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt YONES, Doaa , GALAL، Lamia نويسنده Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt GALAL, Lamia , HUSEEIN، Enas نويسنده Department of Parasitology, Faculty of Medicine, Assiut University, Assiut, Egypt HUSEEIN, Enas
Background: In an effort to understand what limits the virulence of malaria parasites in relation to the host genetic and immunogenic background, we investigated the possibility that the parasite and host genotype crossover interactions constrain virulence.
Methods: Two groups of mice from different genotypes were used (C57BL/6 (B6) and DBA/2 mice). The mice were infected with a virulent parasite line Plasmodium yoelii17XL (P. yoelii17XL). Parasitemia, hematocrit value and lymphocytes yielded by livers and spleens were evaluated. Fluorescence Activated Cell Sorting (FACS) analysis illustrated phenotypic characterization of lymphocytes.
Results: Infection with P. yoelii17XL did not result in thedeath of DBA/2 mice. In contrast,B6 mice developed significantly high parasitemia and succumbed to death. Using (FACS) analysis, DBA/2 mice were found to experience a marked expansion of interleukin (IL)-2Rb+ CD3int cells and gd T cells in the liver, especially in the recovery phase. The expansion of unconventional T cells (i.e. B220+ T cells) was also marked in DBA/2 mice.
Conclusion: The outcome of murine malaria infections depends on the dynamic interplay between the immune-mediator and the genotype of the host.