Fine structural demonstration of cytoplasmic protrusions (Filopodia) in trypanosomes

Macadam, R. F.; Herbert, W.J.

doi:10.1016/s0014-4894(70)80002-9

Cited by 23 publications

(9 citation statements)

References 8 publications

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“…It has been shown that T. brucei [39] and T. congolense [40] isolated from infected blood can have cleavage products of complement component C3 on their surface. T. brucei [41, 42] as well as T. congolense [43] have been observed to form filopodia. Immune complexes of anti-VSG antibody and complement have been shown to be shed via filopodia [43], which, in turn, can be taken up by macrophages [44].…”

Section: Discussionmentioning

confidence: 99%

Intradermal Infections of Mice by Low Numbers of African Trypanosomes Are Controlled by Innate Resistance but Enhance Susceptibility to Reinfection

Wei¹,

Bull

Zhou

et al. 2011

The Journal of Infectious Diseases

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Antibodies are required to control blood-stage forms of African trypanosomes in humans and animals. Here, we report that intradermal infections by low numbers of African trypanosomes are controlled by innate resistance but prime the adaptive immune response to increase susceptibility to a subsequent challenge. Mice were found 100 times more resistant to intradermal infections by Trypanosoma congolense or Trypanosoma brucei than to intraperitoneal infections. B cell–deficient and RAG2−/− mice are as resistant as wild-type mice to intradermal infections, whereas inducible nitric oxide synthase (iNOS)−/− mice and wild-type mice treated with antibody to tumor necrosis factor (TNF) α are more susceptible. We conclude that primary intradermal infections with low numbers of parasites are controlled by innate defense mediated by induced nitric oxide (NO). CD1d−/− and major histocompatibility complex (MHC) class II−/− mice are more resistant than wild-type mice to primary intradermal infections. Trypanosome-specific spleen cells, as shown by cytokine production, are primed as early as 24 h after intradermal infection. Infecting mice intradermally with low numbers of parasites, or injecting them intradermally with a trypanosomal lysate, makes mice more susceptible to an intradermal challenge. We suggest that intradermal infections with low numbers of trypanosomes or injections with trypanosomal lysates prime the adaptive immune system to suppress protective immunity to an intradermal challenge.

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Section: Discussionmentioning

confidence: 99%

Intradermal Infections of Mice by Low Numbers of African Trypanosomes Are Controlled by Innate Resistance but Enhance Susceptibility to Reinfection

Wei¹,

Bull

Zhou

et al. 2011

The Journal of Infectious Diseases

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“…The emission of filopodia by the African trypanosomes has been described by several researchers since the 1970s in infections caused by T. b. brucei and T. b. rhodesiense [25] and African isolates of T. vivax [26] and T. venezuelense ( T. evansi ) [27]. Furthermore, their involvement in the adhesion of T. vivax to the proboscide of Tsetse fly ( Glossina fuscipes ) has been documented [28].…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma vivax Adhesion to Red Blood Cells in Experimentally Infected Sheep

Boada-Sucre

Spadafora

Tavares-Marques

et al. 2016

Pathology Research International

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Trypanosomosis, a globally occurring parasitic disease, poses as a major obstacle to livestock production in tropical and subtropical regions resulting in tangible economic losses. In Latin America including Venezuela, trypanosomosis of ruminants is mainly caused by Trypanosoma vivax. Biologically active substances produced from trypanosomes, as well as host-trypanosome cellular interactions, contribute to the pathogenesis of anemia in an infection. The aim of this study was to examine with a scanning electron microscope the cellular interactions and alterations in ovine red blood cells (RBC) experimentally infected with T. vivax. Ovine infection resulted in changes of RBC shape as well as the formation of surface holes or vesicles. A frequent observation was the adhesion to the ovine RBC by the trypanosome's free flagellum, cell body, or attached flagellum in a process mediated by the filopodia emission from the trypanosome surface. The observed RBC alterations are caused by mechanical and biochemical damage from host-parasite interactions occurring in the bloodstream. The altered erythrocytes are prone to mononuclear phagocytic removal contributing to the hematocrit decrease during infection.

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“…If, however, all the trypanosomes in the blood are equally capable of division, it is not easy to envisage how some of them are destroyed and others perpetuate the infection, for all should be carrying an equal load of antibody molecules. Individual trypanosomes must, therefore, either divide at different rates, or be damaged differentially by antibody or, perhaps, vary in their capacity to shed such molecules, possibly via plasmanemes (Macadam & Herbert 1970). Such differences may have relevance to the problem of explaining the sequential appearance and exponential growth of one, or a few, VATS at each relapse, when many other types are simultaneously present, in small numbers, throughout the infection (Van Meirvenne et al 1975b).…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma brucei: the mechanism of remission in murine infections. A calculator simulation

Herbert

1982

Parasite Immunology

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A simulation (using an electronic calculator program) of the growth of Trypanosoma brucei in the mouse is presented. This suggests that remission of the infection is effected by the removal of ever increasing numbers of the organisms as the immune (antibody) response develops, rather than that a gradual build-up of antibody on each trypanosome occurs until a fatal concentration is reached, simultaneously, on all of them. The program has enabled a theoretical examination to be made of the effect, on the trypanosome growth curve, of altering the doubling time of the organism, the rate of development of the immune response, and the efficiency of the antibodies. Suggestions are made for further extensions of the program to cover other parameters that may vary during the infections. It should also be possible to use similar simple programs, that do not employ advanced mathematics, to problems of the growth of many organisms.

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Fine structural demonstration of cytoplasmic protrusions (Filopodia) in trypanosomes

Cited by 23 publications

References 8 publications

Intradermal Infections of Mice by Low Numbers of African Trypanosomes Are Controlled by Innate Resistance but Enhance Susceptibility to Reinfection

Intradermal Infections of Mice by Low Numbers of African Trypanosomes Are Controlled by Innate Resistance but Enhance Susceptibility to Reinfection

Trypanosoma vivax Adhesion to Red Blood Cells in Experimentally Infected Sheep

Trypanosoma brucei: the mechanism of remission in murine infections. A calculator simulation

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