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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work characterizes the erythropoietic interplay of the spleen, blood, and bone marrow in a lethal murine malaria, strain 17XL P. yoelii. This malaria runs a fulminant 7 day course in BALB/c/ByJ mice, marked by high levels of parasitized reticulocytes with death likely due to anemia. We have quantitated the levels of burst forming units-erythroid (BFU-E), the early, niche-seeking, largely erythropoietin-unresponsive erythropoietic precursors, and of colony forming units-erythroid (CFU-E), the more differentiated sessile erythropoietin-responsive precursors, in bone marrow, blood, and spleen, through the course of this malaria. A decline in marrow BFU-E began on day 2, but recovered, relatively, after day 3. Marrow cellularity declined, being but 75% normal on day 6. Spleen weight increased about 5-fold within 6 days with enlargement of erythroid, lymphoid, macrophage, and stromal compartments. Splenic BFU-E increased in the first 24 hr and 5-fold by day 6. Splenic CFU-E increased in the first 24 hr and into day 4. They then declined and showed a secondary, large-scale, sustained rise interrupted by death. Because the spleen was enlarging, a greater than 60-fold increase in the absolute number of splenic CFU-E occurred at the time of death. Marrow CFU-E followed the same pattern as splenic CFU-E, but the terminal increase represented but a 4-fold absolute increase because of declining marrow cellularity. High levels of erythropoietin occurred only late in the course of disease, likely in response to profound anemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of splenic control of murine malaria: tissue culture studies of the erythropoietic interplay of spleen, bone marrow, and blood in lethal (strain 17XL) Plasmodium yoelii malaria in BALB/c mice. 277 62

Antibody-dependent cell-mediated cytotoxicity (ADCC) against mouse erythrocytes sensitized with immunoglobulin G was studied in mice with malaria. Spleen cells from mice had enhanced cytotoxic activity early in Plasmodium berghei infection but not later in the disease. Sera from infected animals and partially purified malarial immune complexes inhibited ADCC. In addition, ADCC was diminished in spleen cells from mice infected with the lethal variant of P. yoelii 17x compared with that in mice infected with the nonlethal variant. P. berghei-infected erythrocytes did not release 51Cr when incubated with effector cells unless the erythrocytes were sensitized with antibodies against normal mouse erythrocytes.
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PMID:Variation in expression of antibody-dependent cell-mediated cytotoxicity in rodents with malaria. 304 77

Spleen cells from mice immune to Plasmodium berghei exhibited a significantly increased in vitro proliferative response to parasitized reticulocytes compared to spleen cells from normal mice. The specific response to malaria antigen was decreased in spleen cells from pregnant immune mice in contrast to the nonspecific response to the mitogen phytohemagglutinin. Addition of mouse serum to spleen cell cultures of immune mice depressed both the phytohemagglutinin and the specific proliferative response, whereas serum of pregnant mice exerted an even stronger inhibition than serum of nonpregnant mice. Charcoal adsorption of mouse sera for the elimination of steroid hormones removed the serum dependent immunosuppression from normal as well as pregnant serum. Corticosterone added to the spleen cell cultures depressed also the proliferative response. These findings demonstrate that the response to malaria antigen is decreased in immune mice during pregnancy. The possible effect of serum corticosterone on the depression of the immune response is discussed.
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PMID:Plasmodium berghei: reduction of the mouse's specific lymphoproliferative response in relation to corticosterone and pregnancy. 352 63

The in vivo primary antibody response to sheep erythrocytes (SRBC) was determined in genetically resistant C57BL/6 and susceptible A/J mice during the course of infection with Plasmodium chabaudi. Spleen cells from both strains of mice, immunized with SRBC and infected on the same day, showed significant increases in the number of direct plaque-forming cells. The response of malaria-infected C57BL/6 mice was significantly enhanced in comparison with the responses of both normal C57BL/6 and malaria-infected A/J mice. When mice were immunized at later times in the infection, the level of the response declined in both strains until it was less than 50% of the response of normal mice. Thus, suppression of the primary antibody response to SRBC does not correlate with the outcome of P. chaubaudi infection in genetically resistant and susceptible hosts.
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PMID:Modulation of primary antibody responses to sheep erythrocytes in Plasmodium chabaudi-infected resistant and susceptible mouse strains. 377 Sep 56

The thymus-independent antibody response to the alpha 1-6 epitope of dextran B512 was depressed strongly during acute non-lethal Plasmodium yoelii yoelii malaria, but not during low-grade chronic Plasmodium berghei infection. In the acute infection, which is self-limiting, the duration of severe immunodepression was short and was seen only in mice immunized at or around the time of peak parasitaemia. Mice primed at this time responded normally to challenge 20 days later: thus the primary exposure to dextran had no apparent tolerogenic effect. Spleen cells from the immunodepressed mice responded well after transfer to non-infected irradiated hosts, and did not interfere with the adoptive response of normal cells; this, and the fact that P. y. yoelii induced immunodepression in T cell-deprived mice, suggested that T suppressors were not involved. Lack of accessory function, and possibly active suppression, by macrophages remain the most probable explanation for the effect of malaria infection on T-independent antibody responses.
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PMID:Immunodepression of thymus-independent response to dextran in mouse malaria. 616 86

The intraerythrocytic development of malaria parasites results in considerable modification and destruction of erythrocytes. This may lead to the breaking of tolerance such that immune recognition of 'self' or 'modified self' erythrocyte antigens by B or T lymphocytes occurs. Such recognition may be a vital factor in the induction of protective immunity even though it may also cause immunopathology. Serological and immunocytochemical assays have been used to demonstrate, in the serum of Plasmodium berghei-infected or immune rats, antibodies to isoantigenic determinants on infected erythrocytes. Absorption studies indicated that antigens specifically associated with parasitized erythrocytes and erythrocyte isoantigens were closely associated at the surface membrane. Extensive erythrocyte modification and destruction, artificially generated by phenylhydrazine treatment, significantly enhanced immunity against rodent malaria. In contrast, the generation of an incomplete anti-erythrocyte autoantibody response in mice by the injection of cross-reacting rat erythrocytes failed to augment protective responses to P. chabaudi. The reinjection of rat erythrocytes into mice previously injected with rat erythrocytes suppresses further autoantibody synthesis and the mice revert to the normal (Coombs-negative) state. Spleen cells from rat erythrocyte-treated mice transfer this suppression when injected into syngeneic recipients. Coombs-negative mice reinjected with rat erythrocytes failed to show enhanced protective responses to P. chabaudi. Spleen cells from such Coombs-negative mice, injected into sublethally irradiated recipients, increased the protective effects of concurrently transferred spleen cells from malaria-immune donors when the recipients were challenged with P. chabaudi.
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PMID:Protective immunity to malaria and anti-erythrocyte autoimmunity. 634 Sep 99

Spleen cells of BALB/c mice that were immune to the 17X strain of P. yoelii were fused with P3X63Ag8 myeloma cells. Two hundred fifty-three of 1053 hybrid cells produced antibodies reactive with disrupted 17X parasites in a solid phase radioimmunoassay. One of these antibodies, McAb 302, reacted with the merozoites of the 17X (nonlethal) and 17XL (lethal) variants of P. yoelii. Of greater significance, McAb 302 passively protected mice against challenge infection with the lethal variant. Mice treated with this antibody before infection developed low-grade parasitemia (less than 0.3%) of short duration when challenged with P. yoelii 17XL . In contrast, control mice that had been untreated or injected with ascites fluid lacking McAb 302 uniformly died with fulminating malaria upon challenge with the same parasite. In other experiments, McAb 302 was shown capable of controlling blood parasite levels when administered to mice with patent P. yoelii 17XL infections. Although all control mice died, mice protected with a single dose of McAb 302 ultimately cleared their infections. Regardless of how passive immunization was performed, mice given McAb 302 were resistant to subsequent challenge with P. yoelii 17XL , indicating they had developed significant immunity during their initial controlled infections. McAb 302 also showed pronounced passive protective activity against the nonlethal 17X strain of P. yoelii, which is a parasite of reticulocytes. The protection afforded by McAb 302 was specific, because mice passively immunized with this antibody died when challenged with the unrelated P. vinckei. McAb 302 was shown to possess the IgG3 isotype and precipitated a 230-kd protein plus several smaller polypeptides from metabolically labeled parasite antigen preparation derived from both variants of P. yoelii. It did not react with similar preparations of other murine plasmodial species.
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PMID:Passive immunization against murine malaria with an IgG3 monoclonal antibody. 672 50

A comparative study of non-specific immunosuppression by malaria has been carried out in five situations: in both unvaccinated and vaccinated mice infected with the lethal Plasmodium yoelii or the lethal Plasmodium berghei, and in the unvaccinated non-lethal P. yoelii infection. Spleen cells showed a suppressive effect on the normal blastogenic response to mitogens. This suppression was strongest in the mice vaccinated before infection with the lethal P. yoelii and in those infected with non-lethal P. yoelii, suggesting that the suppressive effect did not interfere with recovery. Silica, anti-Thy-1, and indomethacin treatment suggested that this suppression was caused by macrophages. However, the plaque-forming cell response to sheep RBC in vivo was suppressed equally in every case at the peak of the parasitaemia, whereas the suppression of contact sensitivity to oxazolone was strongest in mice with fatal infections. We suggest that different suppressor mechanisms operate in malaria, some being harmful to the host and others possibly beneficial.
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PMID:Two distinct types of non-specific immunosuppression in murine malaria. 701 9

The relationship between splenomegaly and visceral leishmaniasis (VL) was investigated during a cross-sectional study in 2,941 individuals in Baringo District, Kenya, where both malaria and VL are endemic. Spleen size was correlated with presence of malaria parasites in thick blood films and with evidence of present or past Leishmania donovani infection as determined by serology and history. Marked splenomegaly (Hackett grade 3 or greater) significantly correlated with present or previous leishmanial infection (chi 2 = 53.5; p < 0.001) whereas moderate splenomegaly (Hackett grade 1 or 2) significantly correlated with malaria parasitaemia (chi 2 = 73.03; p < 0.001). The presence of antimalarial antibodies did not contribute to the differentiation of the cause of splenomegaly. The diagnostic significance of splenomegaly in this population is discussed.
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PMID:Splenomegaly in Baringo District, Kenya, an area endemic for visceral leishmaniasis and malaria. 748

A longitudinal study was conducted from January 1991 to January 1992 on the Urupa farm, a rural agro-industrial forestry settlement in Rondonia state (Western Amazon Region, Brazil) to define the parasitologic and clinical profile of malaria. Three cross-sectional, parasitologic, and clinical surveys were performed. In the intervals between surveys, malaria cases were monitored by twice a week medical visits to the farm and permanent local surveillance. The population of residents was approximately 170 and was characterized by high mobility. The slide positive rates found in the cross-sectional surveys were 0.5, 4.2 and 2.1, respectively, for the total population (Plasmodium vivax plus P. falciparum). Spleen rate values in children 2-9 years old were always less than 1%. However, this basically hypoendemic malaria situation was unstable, with occurrence of a typical epidemic outbreak at the end of the dry season. The total number of malaria cases recorded from January to December 1991 was 163, giving an annual parasite index of 970 per 1,000 inhabitants. However, sex and age distribution of cases showed rare incidence of malaria in infants and low incidence in children less than the age of 10. Male adults 16-40 years of age represented the main risk group. The observed clustering of cases allowed us to identify the place of work as a factor responsible for high incidence of malaria among adults. The general epidemiologic profile indicated that indoors transmission of malaria by the local Anopheles vector was low or absent.
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PMID:Unstable hypoendemic malaria in Rondonia (western Amazon region, Brazil): epidemic outbreaks and work-associated incidence in an agro-industrial rural settlement. 805 11


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