Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immune response of BALB/c mice to type III pneumococcal polysaccharide (SIII), as measured by splenic PFC, was abolished at the height of an acute self-limiting attack of malaria caused by the murine plasmodium P. yoelii, over a wide range of antigen doses. The response to antigen, given at various times after clinical recovery, gradually reappeared, but did not reach normal levels until 12 weeks after the injection of the parasite. A second injection of P. yoelii given 1 hr before SIII caused a moderate degree of depression, although in this case the plasmodium does not multiply. In chronic malaria the response to SIII was also very poor. Short term under-nourishment was found to reduce only slightly the response to SIII.
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PMID:The immune reponse to type III pneumococcal polysaccharide in mice with malaria. 1 12

Acute Plasmodium yoelii yoelii and chronic Plasmodium berghei malaria infections of CBA mice were accompanied by a reduced capacity to give an antibody response to type III pneumococcal polysaccharide (SIII). The depression of response initiated by acute malaria persisted for several weeks after recovery from clinical infection. During chronic infection, and at the peak of acute parasitaemia, virtually no response to SIII was detected. A substance which crossreacted serologically with SIII was found in blood cells of infected mice. The results suggest that antigen-specific, as well as non-specific, factors may contribute to the depression of the response to this antigen.
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PMID:Immunosuppression in murine malaria. I. Response to type III pneumococcal polysaccharide. 6 96

51Cr studies showed that after complete eradication of malarial parasites erythrocyte life-span is reduced for 4-5 weeks and that the reduction is associated with the presence of complement-containing immune complexes on the red-cell surface. The rate of erythrophagocytosis in the spleen is increased during this period. 59Fe studies of erythropoiesis indicated a mild degree of marrow depression. A very important factor causing anaemia in malaria appears to be a complement-mediated immune process.
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PMID:Cause of anaemia in malaria. 8 77

Invasion of erythrocytes by merozoites of the monkey malaria, Plasmodium knowlesi, was investigated by electron microscopy. The apical end of the merozoite makes initial contact with the erythrocyte, creating a small depression in the erythrocyte membrane. The area of the erythrocyte membrane to which the merozoite is attached becomes thickened and forms a junction with the plasma membrane of the merozoite. As the merozoite enters the invagination in the erythrocyte surface, the junction, which is in the form of a circumferential zone of attachment between the erythrocyte and merozoite, moves along the confronted membranes to maintain its position at the orifice of the invagination. When entry is completed, the orifice closes behind the parasite in the fashion of an iris diaphragm, and the junction becomes a part of the parasitophorous vacuole. The movement of the junction during invasion is an important component of the mechanism by which the merozoite enters the erythrocyte. The extracellular merozoite is covered with a prominent surface coat. During invasion, this coat appears to be absent from the portion of the merozoite within the erythrocyte invagination, but the density of the surface coat outside the invagination (beyond the junction) is unaltered.
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PMID:Erythrocyte entry by malarial parasites. A moving junction between erythrocyte and parasite. 9 21

A distinctive type of hereditary ovalocytosis has been found in Papua New Guinea and a few areas of Southeast Asia. Its main features include a high incidence among tropical lowland dwellers, autosomal recessive inheritance, specific depression of a number of red cell antigens, a characteristic morphology in blood films, and an effect on the erythrocyte sedimentation rate. Speculation has occurred as to whether the high incidence of ovalocytosis in malarious areas may be related to a selective advantage possessed by ovalocytics with regard to severe malaria. Preliminary data tend to support this hypothesis, but the evidence is not conclusive and much further work is needed.
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PMID:Hereditary ovalocytosis in Melanesians. 26 77

The primary antibody response to alumadsorbed BSA was depressed when initiated during low-grade chronic Plasmodium berghei malaria in mice, as previously reported during acute P.y. yoelii infection. Induction of immunological memory by soluble polymerized BSA was abolished in both infections; in infected hosts this normally immunogenic stimulus resulted in partial tolerance. In contrast to the depression of immune response, neither infection interfered with the induction of low-zone tolerance by monomeric BSA. The rate of non-immune elimination of BSA was found to be normal during acute malaria, and only slightly reduced in chronic infection. These results may be explained in terms of abnormal antigen handling in infected mice, due to some functional defect in macrophages, although this does not seem to be a sufficient explanation for all the phenomena of malaria-associated immunosuppression.
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PMID:Immunosuppression in murine malaria. III. Induction of tolerance and of immunological memory by soluble bovine serum albumin. 37 57

Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.
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PMID:Avian malaria in African black-footed penguins. 52 78

Weight, Height, head circumference, chest circumference, arm circumference and triceps skinfold of 223 children under 5 years from the small Mentawai island Sipora/Indonesia have been measured and related to international standards. Beginning from standard values, the anthropometric data decrease during the first 2-3 years, rising again in the following years. Weight for age is 72% of standard at 24 months and 83% at 5 years, height for age 89% at 30 months and 92% at 5 years, weight for height of the boys 82% at 12 months, of the girls 79% at 24 months and 94% for both at 4-5 years, chest/head ratio 95% at 12 months and 100% at 3-5 years. Arm circumference is 83% at 18 months 100% and above already at 3 years. Therefore, fold regains after the minimum of 90% at 18 months and above already at 3 years. Therefore, muscle growth would predominantly be reduced. The weight gain follows approximately the 3rd centile of english girls with a clear depression between 9 and 30 months. The birth weights of 476 children are 3230 g (boys) and 3120 g (girls). Perinatal mortality is low (2.9%), mortality during the first 5 years between 15 and 24%. In the health centre charts of 126 children under 5 years of a selected village (93% of that age group) 463 treatments in 5 years are recorded. The most frequent diagnoses are diseases of the respiratory tract (38% of all treatments), followed by malaria (23%), diarrhoea (19%), ascaris and hookworm infections (7.6%) and skin conditions (6%). Tuberculosis was the cause of treatment in 1.3%. In spite of the temporary growth retardation, as indicated by the anthropometric values, no cases of clinical Protein-Energy-Malnutrition have been observed. Malaria seems to be holoendemic, since all 223 children had a palpable spleen.
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PMID:[Nutritional status and health status of under-fives of the Mentawai island Sipora (Indonesia) (author's transl)]. 74 10

Malaria-induced immunosuppression has been demonstrated in humans and experimental animals. The suppressed immune response has been suggested to be primarily humoral and not cellular in nature, since classical lymphocytic cell-mediated responses have been reported to be normal. Since previous results have demonstrated that an impairment in macrophage antigen processing may be a contributing factor in malaria-induced immunosuppression, the present studies were conducted to determine if the macrophage/reticuloendothelial system (RES) alteration occurs parallel to the course of the malarial infection and if the impairment in antibody formation is temporally related to the RES alteration. The present study has demonstrated that a profound impairment in splenic direct plaque forming cell (PFC) formation occurs in malaria-infected Balb/c mice which had been immunized with sheep erythrocytes (SRBC) either 2 or 4 days after inoculation with Plasmodium berghei, NYU-2 strain. Serum hemagglutinin titers were significantly depressed in mice which received the SRBC 4 days post-inoculation; however, no alterations in antibody titers were observed in mice immunized with SRBC 2 days post-inoculation. Coincident with the depression of serum antibody titers at the day 4 immunization period was a profound increase in the vascular clearance of 51Cr-SRBC with an enhanced hepatic uptake of the 51Cr-SRBC and a decreased splenic localization of the labelled erythrocytes. It is suggested that a direct vascular exposure of the splenic lymphoid-macrophage elements to the parasite may be responsible for the initial early alterations in the PFC response while the impairment in serum antibody titers and splenic phagocytic activity may be a result of the pathological alterations occurring later in the infection, e.g., tissue anoxia, anemia, and hemolysis.
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PMID:A temporal relationship between reticuloendothelial system phagocytic alterations and antibody responses in mice infected with Plasmodium berghei (NYU-2 strain). 76 77

The dysregulation of the immune response by malaria parasite has been considered as a possible constraint to the effectiveness of malaria vaccination. In spite of the important role interleukin-1 (IL-1) plays on the immunoregulation, and its ability to mimic various features of clinical malaria, reports on IL-1 in malaria are lacking. We found that only 2 out of 35 subjects with acute malaria showed increased levels of serum IL-1 alpha by enzyme immunoassay. To assess whether IL-1 could interfere with T-lymphocyte responses, blood mononuclear cells from patients infected with Plasmodium falciparum, P. vivax, or healthy subjects were cultured with phytohemagglutinin, and lymphocyte proliferation measured 72 h later by 3H-thymidine incorporation. Our data showed that T-lymphocyte responses are depressed both in P. falciparum (10,500 +/- 2,900) and P. vivax malaria (13,000 +/- 3,300), as compared to that of healthy individuals (27,000 +/- 3,000). Addition of IL-1 partially reversed depression of malaria lymphocytes, but had no effect on normal cells. On the other hand, T-lymphocytes from malaria infected-subjects presented a minimal decrease in proliferation, when cultured in the presence of exogenous PGE2. These data indicate the occurrence of two defects of immunoregulation in malaria: a deficiency of IL-1 production by monocytes/macrophages, and an increased resistance of lymphocytes to the antiproliferative effect of PGE2.
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PMID:Cytokines and dysregulation of the immune response in human malaria. 134 9


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