Complement in Acute Experimental Malaria I. Total Hemolytic Activity

Fogel, Bernard J.; Doenhoff, Albert E Von; Cooper, Neil R.; Fife, Earl H.

doi:10.1093/milmed/131.suppl_9.1173

Cited by 20 publications

(6 citation statements)

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“…They interpret the data to suggest that parasite death and erythrocyte destruction may be mediated by generation of reactive oxygen species, such as OH', and that this may be the reason for the destruction of nonparasitized erythrocytes and the endothelial cell damage that is known to occur in malaria. Indeed, the fact that substantial activation of the complement system is occurring in both plasmodial as well as babesial infections (25,26) would be consistent with the idea that complement activation results in leukocytic activation, generation of H202, and its conversion in the presence of ionic iron to OH', and tissue injury.…”

Section: Discussionmentioning

confidence: 72%

“…In a control animal, the ratio (defined as the permeability value) usually fell between 0.15 and 0. 25 Details of this animal model have been recently published (5). When animals were subjected to various therapeutic interventions, the agents were injected intravenously together with CVF or intraperitoneally 10 min before vascular infusion of CVF.…”

Section: Methodsmentioning

confidence: 99%

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Evidence for role of hydroxyl radical in complement and neutrophil-dependent tissue injury.

Ward¹,

Till²,

Kunkel³

et al. 1983

J. Clin. Invest.

322

108

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Section: Discussionmentioning

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Evidence for role of hydroxyl radical in complement and neutrophil-dependent tissue injury.

Ward¹,

Till²,

Kunkel³

et al. 1983

J. Clin. Invest.

322

108

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“…Complexes obtained by ultracentrifugation, precipitation with PEG, and filtration through Sephacryl S-300 all significantly inhibited phagocytosis of mouse EIgG (Table 1). Material obtained by sucrose density gradient centrifugation of sera from infected animals obtained on day 21 inhibited phagocytosis of mouse EIgG to 4% of control levels (i.e., ingestion after preincubation of macrophages with PBS) ( Table 1, experiment 1) and to 25% of control levels with sera obtained on day 14 (not shown). Similarly, material obtained by precipitation of serum in 2.5% PEG on day 17 of infection inhibited phagocytosis of mouse EIgG to 33% of control levels ( Table 1, experiment 2), and serum obtained on day 25 inhibited phagocytosis to 4% of control levels (not shown).…”

Section: Resultsmentioning

confidence: 94%

Murine malaria: immune complexes inhibit Fc receptor-mediated phagocytosis

Shear¹

1984

Infect Immun

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Immune complexes have been partially purified from the serum of Plasmodium berghei-infected mice by ultracentrifugation on 10 to 40% linear sucrose gradients, by precipitation with polyethylene glycol, and by gel filtration through Sephacryl S-300. The complexes contain gamma 1, gamma 2a, gamma 2b, and gamma 3 subclasses of mouse immunoglobulin G in differing amounts, as well as malarial antigen. Complexes isolated by all three methods inhibit Fc receptor-mediated phagocytosis by normal mouse peritoneal macrophages but do not inhibit attachment to the Fc receptor or to the C3 receptor or the ingestion of latex particles. The phagocytosis-inhibiting activity of the immune complexes can be partially removed by prior incubation with protein A-Sepharose CL-4B. Splenic macrophages, isolated from P. berghei-infected mice, may be already coated with immune complexes in vivo. Attachment of mouse erythrocytes sensitized with immunoglobulin G to these macrophages is greatly enhanced during malaria, but ingestion is not. These results suggest that immune complexes modulate the immune response to malaria by inhibiting immune phagocytosis and perhaps by interfering with other effector mechanisms. Further understanding of the influence of immune complexes and the antigens involved in these complexes may be useful in vaccine development and prophylaxis.

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“…In 1948 with the use of quantitative assays for C', Dulaney reported a general association of reduced C' in patients with malaria (5). More recent studies in heavily infected monkeys have found a striking depletion of C' shortly before death (6), and variation in C' and C' components levels during schizogony (7). However, no previous reports have related alterations of the C' system in man to the time-course of fever and parasite development during the malarial paroxysm and to malarial immunity. In this study evidence is presented for transitory depletion of C' during paroxysms of vivax malaria when parasitemia is high and antibody is present.…”

Section: Introductionmentioning

confidence: 99%