Trypanosoma musculi infections in complement-deficient mice

Dusanic, Donald G.

doi:10.1016/0014-4894(75)90071-5

Cited by 26 publications

(9 citation statements)

References 5 publications

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“…Targett & Viens (1973) failed to show any lysis of T. musculi in vitro by sera from immune mice. In addition, mice deficient in C5 complement effectively controlled and eliminated the parasites in a manner similar to normal mice (Dusanic 1975, Jarvinen & Dalmasso 1977. These studies would suggest that a trypanolytic system, as originally suggested by Taliaferro (1938), mediated by antibody and complement, is unlikely to play an important role in the killing and elimination of T. musculi.…”

Section: Introductionmentioning

confidence: 52%

“…(1983) demonstrated lytic activity associated with the late stage of infection and involving platelets, immune serum or both. However, C5-deficient mice are as capable of controlling a T. muscufi infection as are normal mice (Dusanic 1975). Also, T. lewisi was not lysed in diffusion chambers implanted in the peritoneal cavity of rats immune to this parasite (Ferrante & Jenkin 1978).…”

Section: Discussionmentioning

confidence: 97%

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The role of the macrophage in immunity to Trypanosoma musculi

Fèrrante

1986

Parasite Immunology

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Trypanosoma musculi was killed by adherent peritoneal exudate cells which had the typical appearance of macrophages. Observations by light and electron microscopy showed that the trypanosomes were phagocytozed and killed intracellularly within phagocytic vacuoles of mouse macrophages. Adherence, phagocytosis and killing of T. musculi required the presence of serum from mice immune to this parasite. Phagocytosis and killing of T. musculi was highly dependent on heat-labile factors in immune mouse serum.

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Section: Introductionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 97%

The role of the macrophage in immunity to Trypanosoma musculi

Fèrrante

1986

Parasite Immunology

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“…Similar findings were obtained with T. brucei by MacAskill et al (20), who showed that CVF treatment prevented immune clearance in passively immunized mice. Although CVF also depletes the later complement components, it is unlikely that these are involved in parasite elimination; Dusanic (7) and others (16) have shown that the course of T. musculi infection in inbred, C5-deficient mice is not significantly different from that in normocomplementemic mice and have concluded that complement-dependent, antibody-mediated cytolysis is probably not a major mechanism for the elimination of T. musculi by the infected mouse. Again, MacAskill et al (20) demonstrated similar findings for T. brucei infections in mice.…”

Section: Resultsmentioning

confidence: 99%

Characterization of antibodies mediating protection and cure of Trypanosoma musculi infection in mice

Wechsler¹,

Kongshavn²

1985

Infect Immun

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Plasma samples were collected from mice infected with Trypanosoma musculi at different times postinfection and administered to naive recipient mice either before or during T. musculi infection. The protective and curative activities of these plasma samples were shown to increase as the time of collection postinfection increased; plasma collected at 14 days postinfection was partially protective and partially curative, whereas that collected at 28 days postinfection was completely protective and curative. The curative activity was labile to heat treatment (30 min at 56°C), whereas the protective activity was heat stable. Additional kinetic parameters relating to the efficacy of protection were investigated. Evidence is presented that both activities are immunoglobulin in nature. Protein A-Sepharose chromatography indicated that the activities are associated with the immunoglobulin G2a or immunoglobulin G3 subclasses of immunoglobulin G. The curative antibody appears to be intrinsically heat labile, since heat treatment of a purified immunoglobulin preparation abolished the ability to cure. Studies on the mechanism of parasite elimination from blood suggest that the process not only requires antibody but is also complement dependent.

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“…In normocomplementemic mice, a trypanolytic mechanism mediated by the late-acting complement components is responsible for killing at least some of the parasites (8). Another pathway apparently exists, however, which is crucial for trypanosome elimination in CS-deficient mouse strains (4). Previous studies in our laboratory have established that three components are essential for this pathway, namely, specific immunoglobulin G2a antibodies, complement component C3, and an effector cell which has not been identified (32)(33)(34).…”

mentioning

confidence: 99%

Cells within the vascular system capable of mediating trypanocidal activity in vitro

et al. 1991

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Cure of Trypanosoma musculi infection involves an effector mechanism mediated by immunoglobulin G2a antibody, C3, and an unidentified effector cell. In the present study, experiments were designed to identify the cell(s) within the vascular system that may be responsible for cure of trypanosomiasis. The ability of various cell populations to mediate killing of trypanosomes in the presence of C3 and immune plasma (IP) was tested in vitro. Blood-derived platelets or leukocytes or Bio-Gel-elicited macrophages or neutrophils were incubated at various concentrations with T. musculi, C3, and IP diluted up to 1 in 8. Trypanocidal activity was dependent upon the presence and concentration of IP and on the number of cells in the wells. Macrophages, neutrophils, and platelets were shown to kill with different potencies. With a 2:1 cell-to-parasite ratio, both macrophages and neutrophils reduced parasite numbers by 2 log, while platelets at a 40:1 ratio mediated a 1 log decrease. In addition, even in the absence of C3, the phagocytes were capable of killing trypanosomes while platelet trypanocidal activity was abrogated. The time course of trypanocidal activity was monitored for macrophages and neutrophils. The number of parasites decreased by 0.5 log by 4 h and 1 to 2 log by 8 h and by 20 h was reduced to zero. Cultured monolayers of endothelial cells were also tested for trypanocidal activity and shown to kill the parasites in the presence of IP and C3. The level of trypanocidal activity was dependent on the concentration of IP.

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Trypanosoma musculi infections in complement-deficient mice

Cited by 26 publications

References 5 publications

The role of the macrophage in immunity to Trypanosoma musculi

The role of the macrophage in immunity to Trypanosoma musculi

Characterization of antibodies mediating protection and cure of Trypanosoma musculi infection in mice

Cells within the vascular system capable of mediating trypanocidal activity in vitro

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