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

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 nonspecific B-cell response induced by infecting mice with two nonlethal malaria parasites, Plasmodium chabaudi adami and Plasmodium yoelii, was analyzed in an isotype-specific reverse plaque assay. Our results showed different isotypic patterns in the two infections, although cells secreting immunoglobulin of all isotypes were increased to some extent. P. yoelii induced large increases in secreting cells of all isotypes; IgG2a-secreting cells were increased out of proportion to those of the other IgG classes. P. chabaudi induced large increases in secreting cells of all isotypes except IgG1. In addition, there was not a disproportionate increase in cells secreting IgG2a. The data show that these "polyclonal" responses are different during each infection. There are marked similarities between the distribution of "nonspecific isotypes" and the specific antibodies formed in each infection.
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PMID:Distribution of immunoglobulin isotypes in the nonspecific B-cell response induced by infection with Plasmodium chabaudi adami and Plasmodium yoelii. 388 Nov 90

Murine T cell populations specific for Plasmodium berghei parasites were generated in vitro from BALB/c immune lymph node cells. The malaria-specific T lymphocytes were shown: a) to proliferate specifically in vitro in response to stimulation with P. berghei-infected red blood cells; b) to exhibit the Thy-1+, Lyt-1+2- cell surface phenotype; c) to provide specific helper activity for an in vitro anti-hapten (TNP) plaque-forming cell antibody response; and d) to protect P. berghei-infected mice from early mortality due to cerebral malaria.
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PMID:Prevention of cerebral malaria by adoptive transfer of malaria-specific cultured T cells into mice infected with Plasmodium berghei. 622 59

Immunosuppression in malaria has been attributed, in part, to alterations in macrophage function. The present study was undertaken in an attempt to characterize the dysfunction and to determine if it is regional or if it occurs in different populations of macrophages. The resting O2 consumption of either hepatic, splenic, or peritoneal macrophages or polymorphonuclear neutrophils (PMNs) was unaltered by the malaria infection. However, the respiratory burst was significantly enhanced in the three macrophage populations but not in the PMNs. A significant increase in their phagocytic capacity and microbicidal activity was noted for hepatic and peritoneal but not splenic macrophages or PMNs. The malaria-infected mice had a marked decrease in serum antibody and splenic plaque response to bovine serum albumin (BSA) but not to keyhole limpet hemocyanin (KLH). Following an in vitro incubation with BSA, splenic macrophages from infected mice were not able to induce an antibody response when injected into normal mice. However, following incubation with KLH splenic macrophages could induce an adequate response in normal mice. This ability of macrophages from malaria-infected mice to transfer (or induce) a response in normal mice appeared to correlate with the amount of antigen digested, or perhaps retained, by the cells, i.e., BSA digestion was significantly less than KLH. These results indicate that the macrophage dysfunction in malaria is distinct depending on the tissue population that the macrophage is obtained from and that the impaired antibody response may be restricted to antigens requiring macrophage processing.
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PMID:Characterization of macrophage dysfunction in rodent malaria. 638 42

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

Depression in immunological responsiveness was manifested in phase with parasitaemia in rats infected with Plasmodium berghei. The spleen was the most affected organ. The response of spleen cells to phytohaemagglutinin (PHA) and the number of plaque forming cells among spleen cells of rats injected with sheep red blood cells (SRBC), were reduced especially at peak parasitaemia. At the onset of the disease the spleen was activated and the responses were amplified. Antibody titres in the serum revealed basically the same picture. Malaria changed also the dose response to antigens so that an overdose of SRBC that normally causes 'immune paralysis' gave rise to significant numbers of plaque forming cells (PFC) in the spleen even in very sick rats. Infection with P. berghei influenced in different ways the two concurrent infections studied: Trypanosoma lewisi and Nipponstrongylus brasiliensis. The severity of trypanosomiasis was proportional to the P. berghei parasitaemia, while the number of the nematodes was not influenced by the malaria in any case. The immunity against T. lewisi depends on the activity of an intact spleen whereas the immunity against N. brasiliensis depends mainly on the mesenteric lymph nodes. The overall results suggest that in malaria the immunological functions of the spleen are severely impaired.
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PMID:Aspects of immunosuppression during Plasmodium berghei infection in rats. 704 23

We have expressed in Escherichia coli the two N-terminal immunoglobulin (Ig)-like domains of the intercellular adhesion molecule 1 (ICAM-1). The first 188 residues of ICAM-1 were expressed with an N-terminal methionine (MP188) or as a maltose-binding fusion protein which was cleaved with factor Xa (XP188). After refolding, both MP188 and XP188 were active in binding to the leukocyte integrin lymphocyte function-associated antigen 1, which has previously been shown to bind to the N-terminal Ig domain of ICAM-1. The major group of rhinoviruses and malaria-infected erythrocytes bind to distinct sites within the first Ig-like domain of ICAM-1. Both MP188 and XP188 bound to malaria-infected erythrocytes; however, only XP188 inhibited human rhinovirus plaque formation. A product (MdQ1P188) with the initiation methionine fused to residue 2, i.e., with glutamine 1 deleted, inhibited plaque formation. MdQ1P188 was able to induce a conformational change of the virus capsid as shown by conversion of 149S particles to 85S particles, whereas MP188 had no effect. These results show that functionally active fragments of ICAM-1 can be produced in E. coli, that glycosylation is not required for ligand binding, and that the N-terminal residue of ICAM-1 is proximal to or part of the human rhinovirus-binding site.
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PMID:Functional studies of truncated soluble intercellular adhesion molecule 1 expressed in Escherichia coli. 810 Oct 71

The thrombospondin family of molecules is expressed in many different tissues. Its expression is highly regulated by different hormones and cytokines and is developmentally controlled. It can bind to many different cell types, probably via an array of receptors which are similarly regulated. The level of thrombospondins in body fluids and their distribution in tissue change in correlation with various pathological states. It is linked to the growth of primary tumors and to metastasis, to development of the atherosclerotic plaque, to malaria infection and other diseases. The role(s) of thrombospondin(s) are by and large unknown, though specific interaction seem to affect particular cell functions. The wide-spread spatial and temporal regulation, multiple interactions and correlation with major diseases imply important roles in cell function and call for concerted effort to unravel the mystery.
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PMID:The functions of thrombospondin and its involvement in physiology and pathophysiology. 834 80

From August through November 1988, 77,500 patients with fever presented to the municipal hospital and to eight government health centers in Kassala, a town of approximately 400,000 individuals in eastern Sudan. A diagnosis of malaria, based primarily on clinical presentation, was made in 14,395 individuals during this four-month period; fevers of unknown origin were diagnosed in 29 patients. A Bunyavirus that was antigenically similar or identical to Batai virus by complement fixation and plaque-reduction neutralization tests was recovered from two of 196 sera collected from patients with acute fever admitted to the municipal hospital in Kassala in October 1988. IgM antibody against this virus was detected by enzyme-linked immunosorbent assay in 7% of the sera from patients with acute fever tested and IgG antibody was detected in 61%.
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PMID:Isolation of Batai virus (Bunyaviridae:Bunyavirus) from the blood of suspected malaria patients in Sudan. 851 85

A 67-year-old man was referred to us for tonic-clonic convulsions. A review of his history revealed that he had been hospitalized for loss of consciousness, hypotension, and suspected apoplexy at age 67. He had experienced prior tonic-clonic convulsions at age 72 and age 74. He had malaria and tuberculosis in his history but had been otherwise generally well. Physical examination was normal, and his blood pressure was 100/80 mmHg. Laboratory findings were normal except alcalinephosphatase (292 U/l) and gamma-glutamyl transpeptidase(60 U/l). Neurological examination showed alert consciousness, mild upper gaze palsy, slight right-side hemiparesis and left Babinski signs was present. Cranial magnetic resonance imaging showed no abnormality, but cerebral angiography revealed bilateral carotid artery occlusion. There were abundant leptomeningeal anastomoses, and the posterior communicating artery was supplied by the left vertebral artery. Electroencephalography showed a spike wave in the temporal lobe and rebuild-up phenomenon in the right hemisphere. Brain atrophy in the anterior and temporal lobes progressed, and the patient experienced gradual disorientation, delirium and hypobulia. He was eventually bedridden. He also demonstrated repetitive tonic-clonic convulsions. After one convulsion, he remained unconscious and died of pneumonia. Autopsy revealed thickening of the intima and internal elastic lamina in the occluded internal carotid artery. The anterior and middle cerebral arteries showed the same pathological changes. Multiple small infarctions restricted to grey matter were present in the cerebral cortex and may have caused the progressive brain atrophy. There was no myelin pallor in the white matter of the cerebrum. Atherosclerotic changes, senile plaque, and neurofibrillary tangles were seen but were within normal limits. These pathological findings were strongly suggestive of moyamoya disease.
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PMID:[An autopsy case of bilateral carotid artery occlusion with repetitive epilepsy and brain atrophy in a senile patient]. 1068 97


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