The mechanisms of malaria anemia remain incompletely understood although much effort has been put on studies in both human and murine systems. Hematopoiesis is regulated by the proliferation, differentiation and maturation of erythropoietic progenitor cells into erythrocytes and is tightly controlled by a complex communication network of cytokines as signal mediators. The present study used the murine P. yoelii 17XNL malaria model to investigate the profile of cytokines and leukocytes throughout the entire infection. Moreover, malaria induced anemia was studied in comparison with anemia induced by hemorrhage and hemolysis. During the P. yoelii infection, the levels of erythropoietic-related cytokines, such as G-CSF, GMCSF, IL-7, and IL-17, were pronouncedly reduced, while those of regulatory cytokines, such as IL-10 and TNF-alpha, were constantly increased. This cytokine profile corresponded well with the cellular composition during the infection, such as drastically decreased levels of CD4(+) and CD8(+) T cells. The profiles of erythropoiesis or hematopoiesis related cytokines during malarial anemia showed striking differences from those during anemia induced by hemorrhage or hemolysis. This study demonstrates that a markedly dysregulated cytokine network occurred in this murine malaria model, which may open a new window of insight into the mechanisms of malaria related anemia.

IntraerythrocyticPlasmodium parasite proliferation istightly related to disease seriousness. Intraerythrocytic parasite developmentis fundamental to the proliferation of the malaria parasite which is affectedby many factors. Antibodies inhibiting intraerythrocytic parasite growth ordevelopment have been long indicated in protective immune mechanisms,particularly in cooperation with human monocytes. Here, we show that the developmentP. falciparum intraerythrocyticparasite was significantly disturbed by antibodies reactive with theintraerythrocytic parasitic antigen Pf332 by inducing parasites with anabnormal morphology. A synergistic effect in the induction of the abnormal formswas seen when antibodies cooperated with human monocytes. The long period of 48hours intraerythrocytic development provides a greater opportunity for antibodiesto react with the intraerythrocytic antigens than with merozoite stage antigens,which are exposed only for a short period of time.