Related Experiment Video

Updated: Sep 27, 2026

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
12:48

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice

Published on: January 2, 2013

[Role of TNF-alpha and ICAM-1 in pathogenesis of cerebral malaria]

L M Che1, Y X Niu, H Z Li

  • 1Department of Parasitology, Capital University of Medical Sciences, Beijing 100054.

Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi = Chinese Journal of Parasitology & Parasitic Diseases
|February 6, 2003
PubMed
Abstract

Insights

Tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) play key roles in cerebral malaria pathogenesis. Elevated TNF-alpha and ICAM-1 expression in infected mice suggest their involvement in disease development.

Area of Science:

  • Neuroimmunology
  • Parasitology
  • Pathophysiology

Context:

  • Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection.
  • The precise mechanisms underlying CM pathogenesis remain incompletely understood.

Purpose:

  • To investigate the roles of tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) in the development of cerebral malaria.
  • To examine the expression of ICAM-1 on brain microvessel endothelium and serum TNF-alpha levels in a mouse model of CM.

Summary:

  • Infection with Plasmodium berghei ANKA strain in CBA/J mice led to significantly higher serum TNF-alpha levels and increased ICAM-1 expression on brain endothelial cells compared to control groups.
  • Intraperitoneal injection of recombinant TNF-alpha exacerbated CM development and enhanced ICAM-1 expression, indicating a direct correlation.

Impact:

  • Findings suggest that excessive TNF-alpha production may induce ICAM-1 expression on brain endothelial cells, thereby contributing to cerebral malaria.
  • This research provides insights into the molecular mechanisms of CM, potentially guiding future therapeutic strategies targeting TNF-alpha and ICAM-1 pathways.

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