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

This paper describes the characterization of proteinuria in Aotus monkeys infected with quartan malaria (Plasmodium brasilianum), using a micro-disc-electrophoresis system. In the post infection urine samples, increases in total proteinuria, albuminuria and gamma-globulinuria were noted a few weeks after peak parasitaemia. Two new proteins also appeared in the urine of malaria infected animals. These findings are discussed with reference to the belief that the Aotus-P. brasilianum system can be a model for human malaria in renal immunopathology.
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PMID:[Proteinuria in quartan malaria-infected Aotus monkeys]. 5 72

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.
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PMID:Immunobiology of malaria. 43 67

It takes a number of years to develop clinical immunity to malaria and malaria pathology is also most evident a number of years after birth. T cells are known to play an important role in defence from malaria parasites but may also contribute to the disease symptoms associated with malaria. T cells which react against malaria parasites have arisen through stimulation with organisms which cross-react with malaria or through exposure to the malaria parasites themselves and express a memory phenotype (CD45Ro+, CD45Ra-, CD4+). T clones which have arisen through exposure to cross-reactive organisms may be expected to home to the tissues where initial exposure occurred as determined by tissue-specific adhesion molecules on the lymphocyte surface. Such tissues may not be appropriate to parasite killing and localization of T cells in such sites may contribute to the immunopathology of malaria. The sharp increase in immunity and decline in pathology observed in later childhood in malaria endemic areas may result from an increase in the number of T cells induced by the parasite itself (as opposed to cross-reactive organisms). Such T cells may not have a preferential trafficking to other organs and may be more likely to circulate through the spleen. Splenic changes may also allow more malaria-specific T cells to concentrate in the spleen and may facilitate interactions between T cells, monocytes, neutrophils and parasites resulting in parasite death. Whereas cytokines secreted by parasite-reactive T cells in all locations may contribute to cerebral malaria and other forms of pathology, cytokines in the spleen at least, should directly contribute to parasite death.
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PMID:The importance of T cell homing and the spleen in reaching a balance between malaria immunity and immunopathology: the moulding of immunity by early exposure to cross-reactive organisms. 128 42

It is now generally accepted that peripheral blood of humans not exposed previously to malaria contains T cells which proliferate vigorously in response to malaria parasites and antigens. Although it has been claimed that these cells express a memory phenotype, their origin is uncertain. We have examined the phenotype and immunological responses of such cells. We confirm that these cells do express the 'memory phenotype', CD45Ro, in that depletion of such cells, but not of CD45Ra (virgin) cells, abrogates the immune response to malaria parasites. In an effort to define the genesis of these responses, numerous malaria-specific T cell clones have been generated from non-exposed individuals. These were tested for reactivity to a large panel of common bacterial, viral, and fungal pathogenic and non-pathogenic organisms. Most clones proliferated vigorously in response to one or more such organisms, while many clones demonstrated smaller but significant degrees of proliferation in response to many different organisms. Our data offers insights into the maintenance of immunological memory. All clones examined were CD3+, CD4+, CD8-, TCR alpha beta+, and TCR delta-. The ratio of TCR alpha beta+ to TCR delta+ cells among peripheral blood lymphocytes increased during polyclonal culture in the presence of parasite. The high frequency of such cells in peripheral blood (1/800-1/9000), and their response to a wide range of geographically different Plasmodium falciparum isolates and clones by both proliferation and lymphokine secretion (predominantly IFN-gamma) with a high degree of sensitivity (less than 1 parasite/microliters blood in some cases) suggests that these cells must be quickly activated following malaria infection. Their contribution to the outcome of the disease (protection/immunopathology) may be significant.
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PMID:'Natural' T cells responsive to malaria: evidence implicating immunological cross-reactivity in the maintenance of TCR alpha beta+ malaria-specific responses from non-exposed donors. 139 Apr 41

In the 1990s, malaria worldwide is still the most important infectious disease. In endemic areas mostly children carry the highest burden of morbidity and mortality. Nevertheless an increasing incidence in adults can be expected. Patterns of disease and immunity within a population may be related to host parasite interactions and recent advances in immunology have contributed to a better understanding at the molecular level. Humoral and cellular responses play a major part in the immunity as well as immunopathology of malaria. Due to their extensive adaptive modulation, it will be extremely difficult to expel malaria parasites from their ecological niche. Most approaches of immunization targeted at different parasite stages, interfere with the acquisition of natural immunity and should thus be pursued with great care if implemented in the field.
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PMID:[Malaria: immune mechanisms and immunization]. 145 94

Serum cytokine profiles were evaluated in immunized and nonimmunized human volunteers after challenge with infectious Plasmodium falciparum sporozoites. Three volunteers had been immunized with x-irradiated sporozoites and were fully protected from infection. Four nonimmune volunteers all developed symptomatic infection at which time they were treated. Sera from all volunteers were collected at approximately 20 time points during the 28-d challenge period; levels of IL-1 alpha, IL-1 beta, IL-2, IFN-gamma, tumor necrosis factor-alpha, IL-4, IL-6, granulocyte macrophage-colony-stimulating factor, and soluble CD4, CD8, and IL-2 receptor (sCD4, sCD8, and sIL-2R, respectively) were determined by ELISA. C-reactive protein (CRP) was assayed by radial immunodiffusion. Parasitemic subjects developed increases in CRP and IFN-gamma, with less marked increases in sIL-2R and sCD8; the other cytokines tested did not change. CRP increases were abrupt and occurred at the onset of fever (day 14 after challenge). IFN-gamma increases were also abrupt, preceding those of fever and CRP by one day. Increases in sIL-2R and sCD8 were more gradual. Increases in fever, CRP, IFN-gamma, and sCD8 were concordant in each volunteer. Early IL-6 increases were noted in the protected vaccinees. Thus, after challenge with virulent P. falciparum, unique systemic cytokine profiles were detectable both in immunized, nonparasitemic volunteers and in unvaccinated, parasitemic subjects. The contrasting cytokine profiles in the two groups may relate to mechanisms of protection and immunopathology in experimental human malaria.
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PMID:Serum cytokine profiles in experimental human malaria. Relationship to protection and disease course after challenge. 164 22

Generation of reactive oxygen radicals by peripheral blood monocytes was measured by luminol-dependent chemiluminescence in 23 P. vivax- and 7 P. falciparum-infected patients. The chemiluminescence index (CLI) was not found to be significantly higher in P. vivax-infected cases than in healthy controls. But in patients with P. falciparum infection, the CLI was significantly higher compared to controls as well as to P. vivax-infected patients. In two severe and complicated P. falciparum-infected cases, CLI was found to be higher than in mild cases. As immunosuppression is more marked in falciparum malaria than in vivax cases, the role of oxygen radical generation in immunopathology and causation of immunosuppression in falciparum malaria needs further investigation.
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PMID:Generation of reactive oxygen species by blood monocytes in human Plasmodium falciparum and P. vivax infections. 201 34

There is now significant evidence that tumor necrosis factor (TNF) is involved in the pathogenesis of malaria. We have tested sera from patients presenting with a febrile illness admitted to hospital in Honiara, Solomon Islands, for the presence of TNF, interferon-gamma, and interleukin-1 (IL-1). This study differs from previous reports as the subjects were mainly adults from a semi-immune population living in an endemic area. The results from 2 different commercially-available assays for TNF were compared, and one was found to be superior to the other. Serum TNF concentrations correlated with malarial parasite density and the patients' temperatures, but not with interferon or IL-1. The results are discussed in the context of the immunopathology of this disease.
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PMID:Serum tumor necrosis factor associated with malaria in patients in the Solomon Islands. 212 52

T lymphocyte responses to malaria-specific antigens during acute falciparum malaria were studied to determine host-parasite interaction and its relation to the manifestations of the disease. The results indicate that while there is antigen-specific immunodepression, markedly elevated levels of soluble factors such as IL2 receptor, CD8 antigen and IFN-gamma suggest that there is intense concurrent cellular activation which however does not seem to be effective in controlling the infection. It is proposed that the cellular activation is to a large extent non-specific and polyclonal, and leads to the exaggerated production of cytokines and eventually immunopathology. Various mechanisms of immunodepression are discussed.
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PMID:T cell responses in acute falciparum malaria. 228 44

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


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