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The Liver-Stage Plasmodium Infection Is a Critical Checkpoint for Development of Experimental Cerebral Malaria

Yuko Sato1,2, Stefanie Ries3, Werner Stenzel4

  • 1Parasitology Unit, Max Planck Institute for Infection Biology, Berlin, Germany.

Frontiers in Immunology
|November 19, 2019
PubMed

Insights

Early liver-stage interactions in cerebral malaria (ECM) are crucial. Modulating these interactions with transgenic parasites prevents ECM pathology by altering immune cell responses, revealing a novel checkpoint.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Pathology

Background:

  • Cerebral malaria (ECM) is a severe complication of malaria, with its mechanisms studied in murine models.
  • Understanding ECM pathogenesis is vital for developing effective treatments.

Purpose of the Study:

  • To investigate the role of liver-stage Plasmodium infection in modulating experimental cerebral malaria (ECM).
  • To identify host-parasite interactions during the liver stage that influence ECM development.

Main Methods:

  • Utilized a transgenic Plasmodium berghei parasite line overexpressing profilin for hemocoel sporozoite-induced infection.
  • Compared virulence and pathological outcomes with transfusion-mediated blood infection.
  • Analyzed splenic immune cell expansion, CD8+ T cell accumulation, lymphocyte recruitment, and monocyte populations (CD115+Ly6C+) in the brain.
  • Measured early cytokine induction (IL-10, IL-12p70, IL-6, TNF) during parasite liver-stage emergence.

Main Results:

  • Transgenic parasites abrogated ECM despite full virulence in blood infections, highlighting the liver stage's importance.
  • ECM was prevented despite comparable splenic immune cell expansion and brain CD8+ T cell accumulation.
  • Cerebral vascular damage was absent, and overall lymphocyte recruitment was suppressed in transgenic infections.
  • Maintenance of CD115+Ly6C+ monocytes was observed in transgenic infections, unlike ECM-prone infections.
  • Early induction of specific cytokines (IL-10, IL-12p70, IL-6, TNF) correlated with diminished hepatic immunity.

Conclusions:

  • Clinically silent liver-stage Plasmodium infections critically modulate the onset of experimental cerebral malaria (ECM).
  • Early host-parasite interactions in the liver can dampen subsequent pro-inflammatory responses, influencing ECM occurrence.
  • This study identifies a novel checkpoint in ECM pathogenesis related to early hepatic immunity modulation.
Keywords:
Plasmodiumcerebral malariaexperimental cerebral malarialiver-stagemalariapre-erythrocytic stagesporozoites

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