Abstract:ABSTRACT:The role of the innate immune responses in the acute phase of malaria infection remains unclear. This study aims to investigate the role of macrophages in lethal Plasmodium yoelii 17XL (P.y 17XL) infection. Female BALB/c mice were injected intraperitoneally with clodronate liposomes at -2,0 day before P.y 17XL infection (300μl /mouse/one time) to depleted macrophages in vivo. Control group of mice were injected intraperitoneally with the same volume of PBS liposome at the same time. Subsequently, the mice were intraperitoneally innoculated with 1 × 106 P.y 17XL infected red blood cells. The parasitemia and survival rates were observed. The levels of spleen culture supernatant of IFN-γ and IL-10 were measured by ELISA. The level of NO (NO2-) was measured with the Griess assay. The numbers of F4/80+ macrophages were detected by flow cytometry (FACS). Compared with the control group, the peak parasitemia came out earlier and mice died earlier in macrophages depleted group. On the 0, 3, 5d after infection, the percentage and absolute numbers of macrophages in spleen cells were significantly decreased in depleted group. Spleen culture supernatant of IFN-γ, IL-10 and NO secretion levels decreased significantly. It seemed that depletion of macrophages resulted in accelerating P.y 17XL infection process and affected the outcome of the infection process of P.y 17XL infection in BALB/c mice. Macrophages play an important role in immune protection against P.y 17XL infection in BALB/c mice.