Common strategies to prevent and modulate experimental cerebral malaria in mouse strains with different

Louise M Randall1, Fiona H Amante, Karli A McSweeney

  • 1Queensland Institute of Medical Research, 300 Herston Road, Herston, QLD 4006, Australia.

Insights

Cerebral malaria (CM) is a severe Plasmodium falciparum complication. Depleting regulatory T cells before infection and CD8+ T cells during symptoms attenuated experimental CM in mice, offering potential therapeutic insights.

Area of Science:

  • Immunology
  • Neuroscience
  • Infectious Diseases

Background:

  • Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, causing high mortality and long-term sequelae, particularly in children and non-immune adults.
  • Distinct genetic loci influence susceptibility to experimental CM (ECM) in different mouse strains, such as CBA/CaH (CBA) and C57BL/6 (B6).

Purpose of the Study:

  • To analyze genome-wide expression profiles in brain tissue of B6 and CBA mice with ECM to identify strain-specific differences.
  • To investigate the impact of regulatory T (Treg) cell and CD8+ T cell depletion on the course of experimental CM in susceptible mouse strains.

Main Methods:

  • Comparative analysis of genome-wide expression profiles in brain tissue from B6 and CBA mice infected with Plasmodium berghei ANKA.
  • Assessment of leukocyte composition, focusing on microglia, in ECM brain tissue.
  • Measurement of serum cytokine levels (interferon-gamma, interleukin-10, interleukin-6).
  • Therapeutic intervention involving depletion of Treg cells before infection and CD8+ T cells after ECM establishment.

Main Results:

  • Significant heterogeneity in gene expression profiles was observed between B6 and CBA mice with ECM.
  • Microglia were expanded in the brain tissue of B6 mice but not CBA mice.
  • Circulating levels of interferon-gamma, interleukin-10, and interleukin-6 were significantly higher in B6 mice compared to CBA mice.
  • Depletion of Treg cells prior to infection attenuated ECM in both mouse strains.
  • Depletion of CD8+ T cells upon appearance of ECM symptoms abrogated ECM in B6 mice and halted its progression in CBA mice.

Conclusions:

  • Experimental CM exhibits significant strain-specific heterogeneity in immune cell infiltration and cytokine profiles.
  • Targeting regulatory T cells and CD8+ T cells represents a promising therapeutic strategy for mitigating experimental cerebral malaria.
  • These findings hold potential implications for developing effective treatments for human cerebral malaria.