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

Histopathological studies in rats and dogs have indicated that hexachlorobenzene (HCB) has immunotoxic properties. Rats exposed to low doses of HCB showed proliferation of high endothelial venules in lymph nodes and accumulation of macrophages in lung alveoli, while lymphoid hyperplasia of the splenic white pulp occurred at higher doses. In dogs, HCB administration produced hyperplasia of lymphoid tissue in the stomach. Functional assessment showed that cell-mediated immunity (delayed-type hypersensitivity response), and humoral immunity (primary and secondary antibody responses to tetanus toxoid) even more, were enhanced in the rat, while macrophage function was unaltered. Stimulation of these immune responses occurred at a dietary level as low as 4 mg/kg HCB following combined pre- and postnatal exposure; at this dose, conventional parameters for hepatotoxicity were unaltered. The developing immune system of the rat therefore seems particularly vulnerable to HCB. In contrast to the immune stimulation observed in the rat, HCB has been reported to suppress the humoral and cell-mediated immunity as well as the resistance to protozoan (malaria and leishmania) infections and to tumour-cell challenges in the mouse; effects have been observed at a dietary HCB level of 5 mg/kg. However, recent data have suggested that HCB has some potential to stimulate the immune system of the mouse also, since increased resistance was shown to a viral infection and to a tumour-cell challenge. Strain differences or the presence of immunosuppressive contaminants in the HCB preparations used do not seem to explain these apparently contrasting results. Although further studies are needed to resolve this discrepancy, current data provide strong enough evidence to classify HCB as a potent immunotoxic chemical.
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PMID:Immunotoxicity of hexachlorobenzene. 329 35

The non-lymphoid elements of the peripheral leucocyte pool were examined in the present study to determine their response to chemotactic stimulation. Our results indicate that granulocytes are effectively mobilized during malaria infections and are not deactivated by complement-derived chemotactic factors. These findings provide further evidence for the restriction of immunosuppression to some specific T and B-cell related functions only.
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PMID:Granulocyte chemotaxis in acute human Plasmodium falciparum malaria. 353 42

The immunology of malaria has been intensively studied, and many reviews of separate topics have appeared. Among host factors contributing to susceptibility to malaria, the following are studied in the present paper: (1) genetic factors affecting susceptibility to human and rodent plasmodia; (2) physiological and nutritional factors affecting susceptibility of vertebrate and vector hosts; (3) sterile immunity in malaria as exemplified by radical cure and by modification of challenge infection following exposure to non-living parasite products; (4) the role of the lymphoid-macrophage system in malaria; and (5) the excessive anaemia of malaria and its etiology.Gamma-globulin levels rise in malaria and remain high during latency. Protection is associated with IgG, which is passively transferable via the human placenta. Not all gamma-globulin is antibody, and not all antibody is protective. The fluorescent antibody technique and double diffusion in gel have been extensively used in exploring the kinetics of antibody production.New methods of harvesting plasmodia attempt to avoid protein degradation and to minimize contamination by host antigens. Plasmodia have proven to consist of a mosaic of antigens, and comparative studies by most of the accepted techniques have been started. Exoantigens have been described in fowl- and rodent-malarias. Relapse-variants of primate plasmodia have been shown to differ antigenically from their parent strains.
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PMID:Current status of the immunology of malaria and of the antigenic analysis of plasmodia. A five-year review. 497 34

In Burkitt's lymphoma, dental structures may provide the route for Epstein-Barr virus (EBV) in saliva to penetrate the jaws, thereby promoting tumor formation. In children, EBV could enter tooth sockets exposed following deciduous tooth loss and thereby contact jaw marrow lymphocytes stimulating neoplastic transformation. Marrow contact by EBV probably also occurs through carious teeth. Jaw tumors are rare in adults because their jaw marrow is no longer hematopoietic and so lacks the lymphoid substrate for the virus. In adults, jaw marrow lymphocytosis, as accompanies infectious mononucleosis and perhaps malaria, or which could develop around the roots of carious teeth having chronic periapical infection, could provide the substrate for EBV. EBV could then contact the jaw marrow lymphocytes when teeth are extracted and so favor jaw tumor development. Therefore, prevention of dental caries might reduce jaw tumor prevalence in Burkitt's lymphoma except among children ages 6-13 whose jaw marrow would unavoidably become infected by salivary EBV when the latter is present at the time of deciduous tooth loss.
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PMID:Circumstances favoring jaw tumors in Burkitt's lymphoma. 632 20

We have isolated, characterized and quantified the immunocompetent cells present in the extravascular hepatic compartment at various stages after Plasmodium yoelii malaria infection with sporozoites. Cytological analyses revealed a predominantly lymphoid population. In mice with a primary infection, the predominant cells were CD4+, CD8+ and B lymphocytes. In fully protected mice, CD3+ CD4- CD8- and polymorphonuclear cells, particularly eosinophils, were most common. The significance of changes in subpopulations is discussed in relation to antigen presentation and host-protective mechanisms.
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PMID:Characterization of liver lymphomyeloid cells in mice infected with Plasmodium yoelii sporozoites. 783 30

Infection with Plasmodium berghei ANKA (PbA) leads, in susceptible strains of mice, to the development of cerebral malaria (CM), a lethal syndrome that reproduces some features of human CM. To study a possible relationship between genetic susceptibility to CM and the cytokine expression pattern, we quantitatively evaluated gene expression on RNA extracted from various organs of malaria-infected mice, using strains that are susceptible and resistant to CM. Northern blot analysis and semi-quantitative PCR showed that CM is associated with an increased TNF-alpha mRNA accumulation in the brain of mice developing the neurologic complications of CM. An increased IFN-gamma mRNA accumulation and a decreased expression of IL-4 and TGF-beta genes were also observed in mice susceptible to CM. In vitro restimulation studies using crude malarial Ag showed that lymphoid cell proliferation was higher in CM-susceptible than in CM-resistant infected mice. Moreover, susceptible mice produced large amounts of IFN-gamma, in a dose-dependent manner, in response to PbA Ag, whereas cells from resistant mice failed to produce significant amounts of this cytokine. Conversely, IL-2 and IL-4 production was significantly higher in infected CM-resistant mouse cells. No difference was seen in the production of IL-3 and IL-5 between resistant and susceptible PbA-infected mice. Upon stimulation with various malarial Ag, comparable amounts of TNF-alpha were produced by macrophages of either strain of mice. Taken together, these findings indicate that susceptibility to CM resides at the level of T cells rather than macrophages. Furthermore, the cytokine production profile is consistent with a predominant Th1-like response in mice developing cerebral complications of malaria.
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PMID:Profiles of cytokine production in relation with susceptibility to cerebral malaria. 840 39

An estimated 300-500 million new infections and 1.5-2.7 million deaths attributed to malaria occur annually in the developing world, and every year tens of millions of travelers from countries where malaria is not transmitted visit countries with malaria. Because the parasites that cause malaria have developed resistance to many antimalarial drugs, new methods for prevention are required. Intraperitoneal injection into mice of one dose of 150 ng (approximately 7.5 micrograms per kg body weight) recombinant mouse interleukin-12 (rmIL-12) 2 days before challenge with Plasmodium yoelii sporozoites protects 100% of mice against malaria. We report that one subcutaneous injection of 10 micrograms/kg recombinant human IL-12 (rhIL-12) 2 days before challenge with P. cynomolgi sporozoites protected seven of seven rhesus monkeys. Protection was associated with marked increases in plasma levels of interferon-gamma (IFN-gamma), and relative increases of lymphoid cell messenger RNA coding for IFN-gamma and several other cytokines. We speculate that rIL-12 protects monkeys through IFN-gamma-dependent elimination of P. cynomolgi-infected hepatocytes. This first report of rIL-12-induced protection of primates against an infectious agent supports assessment of rhIL-12 for immunoprophylaxis of human malaria.
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PMID:Sterile protection of monkeys against malaria after administration of interleukin-12. 898 46

Acute Plasmodium falciparum malaria in African children allows expansion of latent Epstein-Barr virus infection, leading to colonization of lymph nodes by virus-infected lymphoblasts in 60% of cases as demonstrated by in situ hybridization for the detection of EBER-1 and EBER-2 RNA. This probably arises against a background of malaria-induced immunosuppression to EBV and concurrent lymphoid activation. The relevance of the results to the pathogenesis of African endemic Burkitt's lymphoma is discussed.
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PMID:Detection of EBV RNA (EBER-1 and EBER-2) in malaria lymph nodes by in situ hybridization. 944 32

We characterize the mouse gene imap38 and its inducibility by Plasmodium chabaudi malaria among different lymphoid tissues and mouse strains of different H-2 complex and non-H-2 background. Imap38 is a single copy gene assigned to chromosome 6B. It consists of only one exon of 1900 base pairs encoding a highly basic 25.8-kDa protein. Confocal laser scanning microscopy localizes differently tagged IMAP38 proteins in nuclei of transfected cells. Reporter gene assays reveal that the 1730-base pair 5'-flanking region, containing an RSINE1 repeat immediately adjacent to initiation site +1, exhibits promoter activity in nonmurine cells, while it is largely repressed in diverse mouse cell lines, which corresponds to the situation in mouse tissues. P. chabaudi malaria induces imap38 expression almost exclusively in the spleen but not in other lymphoid organs. Parasite lysates are able to induce imap38 in the spleen, but not in spleen cells ex vivo. Activation of spleen cells by LPS and other stimuli is not sufficient to induce imap38. Inducibility of imap38 requires signals from both parasites and the intact spleen, and it is controlled by genes of that non-H-2 background, which also controls development of protective immunity against P. chabaudi malaria.
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PMID:Spleen-specific expression of the malaria-inducible intronless mouse gene imap38. 1044 18

The placenta is an immunologically unique organ where a balance between maternal immunity and fetoplacental well-being must be maintained for successful pregnancy to occur. The intervillous blood is important in this context, yet little is known about local immunologic processes, particularly how placenta-specific memory immune responses are maintained. Using malaria as an illustrative case, we describe an hypothetical model in which recirculation of memory T lymphocytes from the intervillous blood to local lymphoid tissue facilitates maintenance of local memory immunity. This explains how memory cells might be retained when the placenta is expelled at parturition and thus remain available for rapid recall from the local lymphoid tissue to the intervillous space when exposure to the same antigenic stimulus occurs in subsequent pregnancies. Study of cell-mediated immunity to infections like malaria in the intervillous blood and the use of animal models will be necessary to provide proof for this hypothesis.
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PMID:Immunologic memory in the placenta: a lymphocyte recirculation hypothesis. 1078 99


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