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Related Experiment Videos

Interaction between host complement and mosquito-midgut-stage Plasmodium berghei.

G Margos1, S Navarette, G Butcher

  • 1Microbial Immunology Group, Centre for Veterinary Science, University of Cambridge, Cambridge CB3 0ES, United Kingdom. gabi.margos@kcl.ac.uk

Infection and Immunity
|July 12, 2001
PubMed
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Malaria parasites in mosquitoes are initially protected from complement lysis but become sensitive over time. Researchers found that CD59, a key complement inhibitor, is not responsible for this protection.

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Malaria parasite gametocytes transform into extracellular gametes within the mosquito midgut.
  • These gametes are vulnerable to host immune effectors, including complement.
  • Understanding Plasmodium parasite survival mechanisms in the mosquito is crucial for malaria control.

Purpose of the Study:

  • To investigate the role of complement in the mosquito midgut against Plasmodium berghei.
  • To determine the protective mechanisms employed by malaria parasites against complement-mediated lysis.
  • To assess the involvement of host CD59 in protecting gametes from complement attack.

Main Methods:

  • Utilized the rodent malaria parasite Plasmodium berghei and rat complement system.

Related Experiment Videos

  • Analyzed complement component presence (Factor B, D, C3, C5) in mosquito blood meals.
  • Assessed parasite survival rates after complement exposure in vitro.
  • Investigated C3 deposition and CD59 uptake on parasite surfaces using immunofluorescence.
  • Tested the effect of anti-rat CD59 antibodies on parasite lysis.

    • Main Results:

    • Complement components (Factor B, D, C3, C5) are present in the mosquito midgut for hours.
    • Plasmodium berghei gametes show initial resistance (30-50% survival) to complement, increasing sensitivity over time.
    • Parasites showed C3 deposition but lacked uptake of host CD59, indicating CD59 is not the protective factor.

    Conclusions:

    • Malaria parasites develop increasing sensitivity to complement lysis in the mosquito midgut.
    • Host CD59 does not mediate the protection of Plasmodium gametes against complement.
    • Other parasite or host molecules are likely responsible for complement resistance, requiring further identification.