Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alteration of uninfected erythrocytes from Plasmodium (the malaria parasite)-infected blood remained an open question. In this study we compared the in vivo fatty acid compositions of control and uninfected monkey erythrocytes. A large (40%) increase in the linoleic acid level was observed, which was recovered mostly in neutral lipids. An in vitro system was developed to study medium-mediated alterations of cultured erythrocytes by Plasmodium falciparum. The increase in the linoleate level was reproduced in vitro and was also localized in the neutral lipid fraction, especially in triacylglycerols. Studies using proteolytic digestion and heat denaturation showed that a heat-labile serum protein is indispensable for the increase in the linoleate level of red cells treated with the supernatant of P. falciparum cultures. Both the function and the mechanism of this modification of uninfected erythrocytes still remain unknown.
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PMID:Uninfected red cells from malaria-infected blood: alteration of fatty acid composition involving a serum protein: an in vivo and in vitro study. 329 27

An investigation of malariometric indices in relation to immunoglobulin levels, rheumatoid factors, and antithyroglobulins was carried out on 78 members of the Arfak tribe near Manokwari in Western New Guinea, in the course of a WHO assessment of malaria control activities in that region. The population investigated had been exposed to a period of epidemic malaria, as indicated by the small differences in malariometric indices between consecutive age groups. Typically high spleen sizes were recorded, as found generally among Papuans in similar situations. Falciparum malaria was most prevalent, almost equal to cases of vivax and malariae malaria together. IgM levels were very high, while those of IgG, IgA and IgD were not elevated. Total serum protein was rather low. No correlation between malariometric indices, autoantibodies, and immunoglobulin levels could be found. In particular there was no correlation between IgM levels and spleen indices, such as has been found in many other surveys. It is suggested that splenomegaly may show no correlation with the IgM level in Papuan populations without previous selection.
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PMID:Immuno-epidemiology of malaria: a study in a tribal area of West Irian. 421 Oct 55

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T(4)) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T(4) disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-(125)I, followed in 5-7 days by (131)I-T(4) intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound (125)I and protein-bound (131)I, and urinary (125)I and (131)I, together with frequent estimates of serum (127)I-T(4) (Murphy-Pattee) and free T(4) (FT(4)), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of (131)I-T(4) during infection included significant decreases in the fractional disappearance rate for T(4) [(k)], and in the clearance and daily disposal of T(4), all of which returned to control values during convalescence. Total serum (127)I-T(4) increased late in the infected period to become greater during convalescence than either before or during infection, while FT(4) did not increase significantly until convalescence. An analysis of serum (131)I-T(4)/(127)I-T(4) and (131)I-T(4)/PB(125)I ratios confirmed these observations. The slope with time of ratios for urinary (125)I/(131)I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum (127)I-T(4) concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine (125)I/(131)I suggests enhanced thyroidal T(4) secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.
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PMID:Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man. 456 63

1. The major serum proteins which bind halofantrine were identified by size exclusion chromatography. In addition, the binding affinity of halofantrine to human erythrocytes and serum proteins was measured by an erythrocyte partitioning technique. The influence of serum-drug binding on the distribution of halofantrine in whole blood was estimated by simulating several disease-related changes in the levels of the most important binding proteins. 2. The chromatographic resolution of serum preincubated with halofantrine allowed a quantitative analysis of binding to low density lipoproteins, high density lipoproteins, alpha 1-acid glycoprotein and albumin using the erythrocyte partitioning technique. Very low density lipoproteins did not bind halofantrine to a significant extent. 3. In whole blood halofantrine is bound to serum proteins (83%) and to erythrocytes (17%). Low density lipoproteins (affinity constant nKP = 44.4 l g-1) and high density lipoproteins (nKP = 14.4 l g-1) were the most important binding proteins in serum. alpha 1-acid glycoprotein (nKP = 4.39 l g-1) and albumin (nKP = 0.27 l g-1) had relatively low binding affinities. 4. The concentration of serum proteins influences both the fraction of unbound drug and the fraction of drug associated with the erythrocytes. Changes in serum protein concentrations often encountered in malaria are likely to increase both the unbound fraction and the fraction bound to the erythrocytes.
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PMID:The antimalarial drug halofantrine is bound mainly to low and high density lipoproteins in human serum. 766 88

To investigate the pathogenic versus the protective role of cytokines and toxin-binding factors in Plasmodium falciparum infections, we measured the concentrations of tumor necrosis factor alpha, interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-1 receptor antagonist, and IL-6, as well as soluble receptors of tumor necrosis factor and IL-6 (sIL-6R) in serum of Gambian children with cerebral malaria, mild or asymptomatic malaria, or other illnesses unrelated to malaria. Because cytokine secretion may be triggered by toxic structures containing phosphatidylinositol (PI), we also measured concentrations of anti-PI antibodies and the PI-binding serum protein beta-2-glycoprotein I. We found increased concentrations of IL-6, sIL-6R, IL-1ra, and some immunoglobulin M antibodies against PI in children with cerebral malaria, but those who died had decreased concentrations of beta-2-glycoprotein I. We conclude that increased concentrations of cytokines and soluble cytokine receptors represent a normal host response to P. falciparum infections but that excessive secretion of cytokines like IL-6 may predispose to cerebral malaria and a fatal outcome while beta-2-glycoprotein I may protect against a fatal outcome of cerebral malaria.
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PMID:Increased concentrations of interleukin-6 and interleukin-1 receptor antagonist and decreased concentrations of beta-2-glycoprotein I in Gambian children with cerebral malaria. 792 98

The relationship of serum protein polymorphisms to the presence of malaria antibodies was studied in 473 muria gond tribal subjects from Bastar district, Central India, an area endemic for both P. falciparum and P. vivax infection. A control group of 100 subjects in Delhi, which has a low prevalence of malaria, was also studied. Serum proteins (transferrin, haptoglobin and albumin) were analyzed for polymorphic variants by starch gel electrophoresis. Malarial antibodies were assayed by enzyme linked immunosorbent assay (ELISA), while thin blood films were screened for the presence of malaria parasites. Among serum proteins transferrin CD variant showed significant correlation with malarial infection. There were no significant differences observed between Hp1 and Hp2 variants of haptoglobin in relation to presence of malarial antibodies. Statistical analysis for albumin variants was not attempted because the number of individuals showing abnormal bands was small.
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PMID:Serum protein polymorphisms and malaria in Madya Pradesh, India. 826 24

The mannan-binding lectin (MBL) is a serum protein, which is involved in the immune defence against viruses, bacteria and parasites. Children who have mutations in the MBL gene that lead to a MBL deficiency are more susceptible to infectious diseases and are more likely to suffer from severe malaria. In this report we investigate the interaction between MBL and the proteins of red blood cells infected with the parasite Plasmodium falciparum. Protein extracts were separated on MBL-sepharose columns. After the elution of bound material, the proteins were detected either by Western blot with human antibodies, or radioactive labelling with 35S-methionine or 3H-glucosamine. MBL recognises proteins of P. falciparum-infected erythrocytes that are immunogenic in humans, parasite-derived and glycosylated. Whether the proteins identified in the different assays are identical remains to be explored. MBL added to in vitro cultures of P. falciparum, however, does not inhibit parasite growth. The positive effect of MBL in the blood of malaria patients could be caused by detoxification of parasite products.
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PMID:Recognition of plasmodium falciparum proteins by mannan-binding lectin, a component of the human innate immune system. 1193 98

The serum protein patterns of groups of Nigerians including 98 children partially protected by "daraprim" against malaria, and 113 unprotected children, have been studied. The protected children have a significantly lower concentration of serum gamma globulin than the unprotected children from the age of 12 months onwards. In children, sicklers have a significantly higher serum gamma globulin than non-sicklers. It is suggested that sickling protects against malaria by enhancing the antibody response against the malaria parasite.
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PMID:The relationship of serum gamma-globulin concentration to malaria and sickling. 1381 66

Malaria leads to pathophysiological and biochemical alterations in placenta and blood of pregnant mice. A significant decrease in the sugar, protein and lipid levels in the placental homogenate of pregnant-infected mice was observed compared to the pregnant mice. However, serum protein content was not altered much in the pregnant-infected mice as compared to the levels in control mice. The serum lipid level enhanced significantly in both pregnant and non pregnant-infected mice. The enzymatic activities of alkaline phosphatase and acid phosphatase altered significantly in malaria-infected placenta. Our study clearly highlights the possible role of these enzymes in damaging the placenta which in turn may jeoparadise the fetal growth together with altered biochemistry of placenta. Therefore biochemical along with pathological alterations occurring during malaria infection in pregnancy may account for compromised maternal fetal relationship.
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PMID:Plasmodium berghei induced biochemical alterations in pregnant mice. 1759 79

Mannose-binding lectin (MBL) is a serum protein which initiates innate immune responses to microbial pathogens by binding to non-self surface oligosaccharides. MBL deficiency is the most common congenital immunodeficiency of human and has been shown to predispose to infections, particularly in children and immune compromised. In a matched case-control study among 870 Ghanaian children, we examined the influence of six polymorphisms of the MBL2 gene on Plasmodium falciparum infection and severe malaria. A missense mutation resulting in low MBL activity (MBL2*C) was found in 35% of healthy controls, but in 42% of asymptomatically infected children (P=0.01), and in 46% of patients with severe malaria (P=0.007). Heterozygosity for MBL2*C was associated with increased odds of infection (odds ratio (OR), 1.6; 95% confidence interval (CI), 1.1-2.1), severe malaria (OR, 1.7; 95% CI, 1.2-2.4), and of severe anemia in particular (OR, 2.3; 95% CI, 1.4-3.8). The population attributable fraction of severe malaria cases attributable to MBL2*C heterozygosity was 17%. Our results suggest that the MBL pathway of the complement system is a critical determinant of both, susceptibility to P. falciparum infection and manifestation of severe malaria, particularly in young children in whom specific immune responses are weak or absent.
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PMID:Mannose-binding lectin variant associated with severe malaria in young African children. 1839 36


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