Determination of the expression of lymphocyte surface markers and cytokine levels in a mouse model of Plasmodium berghei (original) (raw)
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Clinical & Experimental Immunology
The development of circulating immune complexes was studied in mice of the BALB/c, A/J, OF1, CBA and C57B1 strains infected with P. berghei. Complexes were evaluated in relation to levels of parasitaemia, soluble antigen, specific antibody and C3. Susceptibility to infection was greatest in BALB/c, A/J and OF/a mice. The maximum parasitaemia was 30% in CBA and 70% in all other strains. Levels of soluble antigen paralleled those of parasitaemia. Specific antibody was detected in all strains, but the titre continued to rise throughout the infection only in CBA mice. Circulating immune complexes occurred in mice of all strains from day 6; the level fell after day 9 in C57B1 whereas it was maintained in CBA mice. The development of immune complexes was associated with marked depression of C3 levels in all except CBA mice, in which a transient reduction was followed by recovery. Partial characterization of the complexes showed that IgM-containing complexes appeared earliest and reached h...
Parasitology Research, 2011
To mimic a human malaria infection in the endemic condition, two strains of mice (Balb/c and CBA) were infected and treated several times to generate so-called semi-immune status. As previously reported, neither mice (Balb/c and CBA) strain showed cerebral malaria, even in the susceptible C57BL/6 (B6). The significant difference between the mice strains in our previous study was the rate of destruction of uninfected red blood cells (uRBCs) at infection. After the established repeated cycles of infection and treatment and the final challenge with 104Plasmodium berghei ANKA until minimum Hb, Balb/c and CBA mice were sacrificed. The spleen, liver, brain, kidney, lung, heart, and muscle were removed, stained with hematoxylin–eosin and analyzed with light microscopy. Previous observation suggested that Balb/c destroyed uRBC at much higher rate than the other strains although the parasitemia was very low. Pathological investigation carried out in this study revealed that this destruction was mainly contributed by the uRBCs as no parasite sequestration was observed in any of the organs. However, malaria pigment deposition was observed in spleen and liver of all the semi-immune mice strains. This histopathological study in the severe malaria anemia model, which is difficult to conduct in humans, will be helpful in taking into account different responses to malaria infection when designing therapeutic interventions and vaccine studies.
Immunity to Plasmodium Berghei Yoelii in Mice
The Journal of Immunology
The kinetics of various specific and nonspecific immunologic responses were examined in BALB/c mice infected with 17X nonlethal Plasmodium berghei yoelii (a self-limiting infection). The sequence of events after infection was characterized by rapid sensitization of splenic T cells to malaria antigen and polyclonal B cell activation, followed by a period of depressed splenic proliferative responses in vitro to mitogens (PHA and LPS) and malaria (specific) antigen. At the same time, suppressed primary in vitro splenic PFC responses to trinitrophenyl-aminoethylcarbamylmethyl-Ficoll (TNP-F) were seen. This suppression was an active process requiring adherent cells. During this period, levels of antimalarial antibody also increased exponentially. As the infection was cleared, splenic malaria antigen-specific proliferative responses were again observed and splenic PFC and in vitro mitogen responses returned to preinfection levels after variable periods of time. Both splenic proliferative ...
Cellular changes in the bone marrow of Plasmodium berghei-infected mice
Cellular Immunology, 1980
The present work is concerned with early cellular changes occurring during a malaria infection. Blast transformation by lymphoid cells and phagocytosis by adherent cells from the bone marrow was performed, using immune and nonimmune Balb/c mice. Nonadherent bone marrow cells from immune mice show an increased specific lymphoblast transformation. This increase was not observed during a lethal infection (PI). Adherent bone marrow cells were assayed for phagocytosis of parasitized (PE) or normal erythrocytes (NE). Cells from immune mice show an increase in phagocytosis of PE and NE. Cells from PI mice showed a decreased phagocytosis throughout the infection, beginning at Day 1 after challenge.
Parasite, 2010
In previous studies of the infection of rats by P. berghei Anka, we have shown that primary blood stage infection induced the expansion of CD4+ T cells and CD8+ T cells in adult resistant rats while the number of CD4+CD25+ cells was found to be higher in young susceptible rats. In this work, the respective contribution of each cell population was determined in young and adult rats treated with monoclonal antibodies. Down-regulation of surface CD25 molecules, including those expressed by CD4+ cells did not significantly enhance the capacity of young rats to control the development of erythrocytic stages or modify the course of infection in adult infected rats. However, we observed a significant loss of protection when adult rats were treated with anti-CD4 mAb (W3/25) with higher blood parasitemia levels and 50 % of rats succumbed to infection. More importantly and in contrast to earlier studies performed in mice, we found a significant increase in blood parasite levels and a significant delay in parasite clearance in adult rats treated with anti-CD8 mAb OX8, known to deplete CD8+ cells. These results suggest that CD8+ cells play a critical role in the development of immune responses in rats to control the replication of blood stage parasites. Résumé : LE CONTRÔLE DES FORMES SANGUINES DE PLASMODIUM BERGHEI ANKA CHEZ LE RAT EST DÉPENDANT DES CELLULES CD4+ ET CD8+ MAIS INDÉPENDANT DES CELLULES CD25+ Nous avons précédemment montré que l'infection primaire de rats jeunes/adultes par Plasmodium berghei Anka induisait une expansion des cellules T CD4+ et T CD8+ chez les rats adultes résistants alors que des taux de cellules CD4+CD25+ significativement plus élevés étaient retrouvés chez les rats jeunes susceptibles infectés. Dans ce travail, par des traitements avec des anticorps monoclonaux, nous avons déterminé la contribution de chacune de ces populations cellulaires chez les rats jeunes et adultes au cours de l'infection. Nous montrons ainsi que la diminution de l'expression du marqueur CD25, y compris à la surface des cellules CD4+, ne modifie en rien le déroulement et l'issue de l'infection, que ce soit chez les rats jeunes susceptibles ou chez les rats adultes résistants. À l'inverse, le traitement de rats adultes avec un anticorps monoclonal anti-CD4 (W3/25) induit une augmentation de la parasitémie et ~50 % des rats traités succombent à l'infection. De même, la déplétion des cellules CD8+ chez des rats adultes infectés induit une augmentation de la parasitémie. Ces résultats suggèrent que chez le rat, contrairement à ce qui a été montré chez la souris, les cellules CD8+ jouent un rôle critique dans le développement des réponses immunes impliquées dans le contrôle des stades érythrocytaires du Plasmodium.
Infection and immunity, 1986
Affinity-purified Plasmodium falciparum soluble antigens (SPAg) isolated from in vitro cultures of the parasite were shown to be relatively free of nonspecific polyclonal activators. To determine the presence of lymphocytes with specificity against SPAg in the peripheral blood of malaria-immune individuals, the proliferative response and the interleukin-2 (IL-2) production of SPAg-activated mononuclear cells (MNCs) from individuals unexposed, sensitized, and immune to malaria were measured. It was found that MNC isolated from malaria-immune individuals proliferated in response to SPAg and that this activation resulted in measurable IL-2 production in 5 of 10 MNC cultures. MNC isolates from most unexposed individuals did not respond to SPAg. To establish which cells responded to SPAg, different subpopulations of MNCs were tested. Only T helper cells were found to respond, and they responded only when cocultured with monocytes. The finding of parasite-specific T helper cells in the bl...
Clinical & Experimental Immunology
Histological changes during the course of P. berghei infection were investigated in A/J, BALB/c, OF1, CBA and C57B1 mice. The findings were studied in relation to serological aspects (Contreras et al., 1980). High mortality and acute deaths occurred in A/J, BALB/c and OF1 mice and marked cerebral lesions were found in these strains from day 15, including congestion of meningeal and cerebral veins and capillaries, blocking of these vessels by heavily parasitized RBC, cerebral oedema and haemorrhages. Such lesions were minimal in CBA and C57B1 mice, and absent in mice examined 21 and 24 days after infection. Small deposits of IgG and traces of C3 were detected by immunofluorescence in the choroid plexus of most mice from day 9. Renal lesions included congestion, plugging of veins and capillaries, low-grade mononuclear infiltration and mesangial thickening; these changes were most marked in CBA, C57B1 and A/J mice. Glomerular deposits of IgM were present in all strains in the first wee...
Journal of the National Medical Association, 1979
Malaria, the number one disease in the world, is caused by intracellular protozoans belonging to the Subphylum, Sporozoa; Suborder, Haemosphoridia; and Family, Plasmodiidae. The four classical organisms producing disease in man are Plasmodium vivax, P. falciparum, P. malariae, and P. ovale. Although malaria has been known to man for centuries, attempts are still being made to control and eliminate its devastating effects in tropical and subtropical areas of the world. Current active interest in malarial immunology and immunopathology derives from two main facts: (1) that human malaria is still one of the chief health problems in a broad tropical and subtropical zone in which lie most of the developing countries; and (2) most of the seminal leads in basic immunology are being applied to malarial immunology, either directly in human patients, or using laboratory animals as test objects.This paper addresses the nature of malarial immunity and target organs in malarial pathology.