| PREFACEMalaria is one of three most serious parasite diseases threatening people now. It is the constant blood-stage plasmodium schizont multiplication that results in a series of serious clinical symptoms, and more than 2 million people die from malaria every year. Recently, emerging of new anti-malaria drugs plasmodium and anti-insecticide mosquito results in a increasing tendency of malaria infective patitents. Thus, new prevention and cure provisions involving in developing and producing of malaria vaccines are important and necessary. Further demonstration of host immune response against blood-stage plasmodium, especially , the various protective immunity between the host resistance and plasmodium clearance is premise to the development of the effective malaria vaccines and new anti-malaria drugs.Experimental results suggested that resistant mice and susceptible mice lastly show two very different results; self-resolving and death during the plasmodium infective course. The same experimental animals-mice infected with different strains of plasmodium show different immune responses. And immunity to the same sixain of malaria parasite is significantly different in various genetic background hosts. In this research, we will demonstrate the characteristics of specific immune responses against blood-stage plasmodium and supply a necessary experimental data for developing of the effective malaria vaccines and new anti-malaria drugs.MATERIALS AND METHODSDBA/2 mice were injected intraperitoneally(i. p. ) with erythrocyte ( RBC)suspension containing 106RBC parasitized ( PRBC ) by lethal strain, P. yoelii 17XL. Sera and spleen cell supernatants were collected at 0,1,3,6,9,12,15,20 day and assayed for IFN--y, IL-12, IL4, IL-10,IgG and nitric oxide (NO) respectively. Parasitemia,mononuclear macrophages% and phagocytosis were daily described. Statistical analysis was performed by using Student' s t test. P value of <0. 05 was considered significant.RESULTS1. Levels of parasitemiaPRBC began to emerge in vein blood on day 3 postinfection, which peaked on day 9 postinfection(46. 87% ). Then, levels of parasitemia began to decline after day 9, began to increase again on day 12 postinfection, which peaked on day 15 postinfection (42. 62% ). Parasitemia were cleared by day 20.2. Mononuclear macrophages% and phagocytosisNumbers of monocyte in blood from DBA/2 mice began to increase on day 3 postinfection. From day 6 to day 16, we saw some mononuclear macrophages phagocytosing several plasmodium.3. Levels of cytokines in serum and NO in spleen cell supernatants Levels of IL-12 in serum from DBA/2 mice began to increase on day 1postinfection ( P <0. 05). Levels of IFN-*y in serum from DBA/2 mice were also significantly high,which peaked on day 6 postinfection( P <0. 01). Though levels of IFN-7 in serum from DBA/2 mice decreased somewhat from day 9 to day 20 ,it is very significant compared to that of control mice( P <0. 05 ). Levels of IL-4 and IL-10 in serum from DBA/2 mice began to increase on day 6 postinfection, which respectively peaked on day 9(P <0. 05) and 15 postinfection( P < 0.01). NO production of splenocytes from DBA/2 mice were apparently high from day 6 to 20 postinfection( P <0.01).4. Levels of IgG in serumLevels of IgG from DBA/2 mice serum began to increase after infection, which peaked on day 70 postinfection ( P <0.01).DISCUSSIONPrevious study demonstrated that resistant C57BL/6 mice and susceptible A/J mice lastly show two very different results: self-resolving and death during the P. chabaudi infective course. The defense mechanism of resistant C57BL/6 mice in the early phase of infection with P. chabaudi largely depends on Thl cellular immunity associated with a predominantly IFN-- secretion to inhibit para-sitemia, then switches to antibody-mediated response to clear parasitemia. During P. yoelii 17 XL infective course, DBA/2 mice inhibit parasitemia rapid increasing by establishing Thl cellular immunity and clear plasmodium through effective humoral immu... |
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