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Experimental cerebral malaria develops independently of endothelial expression of intercellular adhesion molecule-1

Theresa N Ramos1, Daniel C Bullard, Meghan M Darley

  • 1Department of Microbiology and Neurology, University of Alabama, Birmingham, Alabama 35294, USA.

The Journal of Biological Chemistry
|March 16, 2013
PubMed

Insights

Full-length ICAM-1 on endothelial cells is not essential for cerebral malaria (CM) development. Instead, ICAM-1-mediated cellular aggregation, independent of brain microvasculature expression, drives experimental CM (ECM) pathogenesis.

Area of Science:

  • Immunology
  • Neuroscience
  • Infectious Diseases

Background:

  • Cerebral malaria (CM) is a severe Plasmodium falciparum malaria complication with high mortality and neurological sequelae.
  • Pathogenesis involves sequestration of infected red blood cells in brain microvasculature via adhesion molecules.
  • Intercellular Adhesion Molecule-1 (ICAM-1) is hypothesized to be crucial on endothelial cells for this sequestration in CM.

Purpose of the Study:

  • To investigate the role of ICAM-1 isoforms in the development of experimental cerebral malaria (ECM).
  • To determine if endothelial ICAM-1 expression is necessary for ECM pathogenesis.

Main Methods:

  • Utilized ICAM-1 mutant mice lacking specific isoforms.
  • Generated transgenic mice expressing ICAM-1 exclusively on leukocytes.
  • Observed and analyzed ECM development and phenotype in these models.

Main Results:

  • The full-length ICAM-1 isoform is not required for murine ECM development.
  • ECM phenotype is influenced by the specific combination of ICAM-1 isoforms expressed.
  • ECM developed in mice expressing ICAM-1 solely on leukocytes, indicating endothelial expression is not essential.

Conclusions:

  • Endothelial cell ICAM-1 is not required for the pathogenesis of experimental cerebral malaria.
  • ICAM-1-dependent cellular aggregation, irrespective of its expression on the cerebral microvasculature, contributes to ECM.
  • Findings suggest alternative mechanisms of ICAM-1 involvement in CM pathogenesis.

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