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Immunopathological changes in human cerebral malaria

J Porta1, A Carota, G P Pizzolato

  • 1Department of Pathology, CMU, University of Geneva, Switzerland.

Clinical Neuropathology
|May 1, 1993
PubMed
Summary
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Cell-mediated immunity and tumor necrosis factor-alpha (TNF) play a role in severe malaria pathogenesis. Autopsy findings reveal leukocytes and TNF alongside infected cells, suggesting immune involvement in cerebral malaria.

Area of Science:

  • Immunology
  • Pathology
  • Neuroscience

Background:

  • Pathogenic mechanisms of human cerebral malaria are not fully understood.
  • Severe malaria involves Plasmodium falciparum-infected erythrocytes sequestering in cerebral vessels.
  • Cell-mediated immunity and TNF are implicated in murine malaria models.

Observation:

  • Autopsy of a cerebral malaria patient revealed classic signs like erythrocyte sequestration, cerebral edema, and Dürck granulomas.
  • Leukocytes expressing CD68 and TNF coexisted with infected erythrocytes in capillaries.
  • Monocytes outnumbered erythrocytes in venules, and ICAM-1 was upregulated on endothelial cells with sequestered cells.

Findings:

  • The observed changes mirror those in murine models, suggesting a similar pathogenic role for cell-mediated immunity and TNF.

Related Experiment Videos

  • In vitro studies show ICAM-1 can bind to P. falciparum-infected erythrocytes.
  • High serum TNF levels correlate with malaria severity and may enhance cell adhesion via ICAM-1.

    • Implications:

    • These findings provide further evidence for the involvement of cell-mediated immunity in human cerebral malaria pathogenesis.
    • Understanding these mechanisms could lead to targeted therapies for severe malaria.
    • The study highlights the potential role of TNF and ICAM-1 in the adhesion of infected cells and leukocytes in cerebral malaria.