Erythrophagocytosis in malaria: Host defence or menace to the macrophage?
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Plasmodium (life cycle)
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Nearly one million people are killed every year by the malaria parasite Plasmodium. Although the disease-causing forms of the parasite exist only in the human blood, mosquitoes of the genus Anopheles are the obligate vector for transmission. Here, we review the parasite life cycle in the vector and highlight the human and mosquito contributions that limit malaria parasite development in the mosquito host. We address parasite killing in its mosquito host and bottlenecks in parasite numbers that might guide intervention strategies to prevent transmission.
Plasmodium (life cycle)
Obligate
Obligate parasite
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Cardioprotection
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The infection of mice and baby rats by both Plasmodium lophurae , an avian parasite, and Plasmodium berghei , a mammalian malaria parasite, prompted investigation of the likelihood of P. berghei infecting avian erythrocytes. Though erythrocytes of chick embryos were not infected, those of the goose and duck embryos were. In both these cells the morphology of the parasite was markedly different from that seen in mammalian erythrocytes. Infections were transitory and it was impossible to find parasites after 4 days. Examination of the hosts of both species of parasites showed a rather wide range and examination of the susceptibility of the duck erythrocyte indicated that this cell was peculiarly receptive to infection by a variety of plasmodia.
Plasmodium berghei
Plasmodium (life cycle)
Avian Malaria
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Abstract Macrophages infected in vitro with murine cytomegalovirus (MCMV) manifest depressed phagocytic uptake of a variety of particles within hours after the initiation of infection. Analysis of kinetics of uptake of radiolabeled Staphylococcus aureus by MCMV-infected macrophages indicates that the diminished uptake results from a depression in the calculated maximum velocity of uptake (Vmax) with the apparent Michaelis constant (KM) remaining unaltered. This pattern of altered uptake is typical of that seen after manipulations that affect the surface interactions of macrophages with ingestible particles. Coincubation of macrophages and radiolabeled Staphylococcus with opsonizing antibody resulted in normalization of the phagocytic rates. The surface localization of the defective phagocytosis was further confirmed by light and scanning electron microscopy of the macrophages incubated with Staphylococcus or latex spherules. These data indicate that defective macrophage phagocytosis induced by MCMV infection results from an aberration in the macrophage surface that interferes with the initial macrophage-particle interactions that initiate nonimmune phagocytosis.
Cytomegalovirus
Antibody opsonization
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In this study, we determine its macrophage phagocytosis in different growth stage of Avian broiler after absorbed water soluble alfalfa polysaccharides (WSAP) by three kinds of method. The result showed: effect of WSAP on the macrophage phagocytosis in broilers isn't obvious, but individual group's effect is obvious.
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Plasmodium berghei
Plasmodium (life cycle)
Lobules of liver
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Inert
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Objective To explore the influence of Pseudomonas aeruginosa(PA) biofilm and alginate on macrophage phagocytosis function in mouse.Methods The bacterial biofilm suspension of PA was used to infect macrophage-depleted mouse and control mouse to explore the influence of biofilm on macrophage.The macrophage was isolated from mouse and added with alginate inside,then the phagocytosis rate was determined.The capability of macrophage's phagocytosis was detected by neutral red method.Results The bacterial count in macrophage-depleted mouse compared to the control group was(4.16±3.36)×105 /ml to(5.15±1.92)×105 /ml,t=0.7211,P=0.483.The phagocytosis rate in PA biofilm group compared to the control group was(13.82±4.71)% to(42.73±11.00)%,Q=12.3231,P0.01.This suggested that the PA biofilm group can be more resistant to macrophage phagocytosis compared to the control group.The phagocytosis rate in alginate group compared to the control group was(22.91±6.20)% to(42.73±11.00)%,Q=8.4465,P0.05.This showed that the alginate group can also be more resistant to macrophage phagocytosis compared to the control group.When the concentration of alginate were 0,25,50,75,100,125 and 150 μg/ml the absorbance A(540 nm)which represents the capability of macrophage phagocytosing neutral red,were(0.271±0.044),(0.456±0.062),(0.445±0.061),(0.551±0.065),(0.210±0.053),(0.186±0.026)and(0.195±0.025)respectively.When the alginate's concentration ≤75 μg/ml,the capability of macrophage phagocytosing neutral red strengthened(P0.05),compared to the 0 μg/ml group;When the alginate's concentration 75 μg/ml,the capability of macrophage phagocytosing neutral red decreased(P0.05),compared to the 0 μg/ml group.Conclusion Macrophage can prevent the invasion of PA.PA biofilm can inhibit macrophage phagocytosis.Alginate can promote macrophage phagocytosis at doses of ≤75 μg/ml while larger doses of alginate inhibit macrophage phagocytosis.
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