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Trypanosoma cruzi-triggered meningoencephalitis is a CCR1/CCR5-independent inflammatory process

Andréa Alice Silva1, Ester Roffê, Helton Santiago

  • 1Laboratory of Autoimmunity and Immunoregulation, Institute Oswaldo Cruz, Fiocruz, Av. Brasil 4365, Rio de Janeiro, 21045900, Brazil.

Journal of Neuroimmunology
|February 6, 2007
PubMed

Insights

Acute Trypanosoma cruzi infection can cause meningoencephalitis, involving CD8 cells and specific cytokine mRNA. However, this inflammation is independent of CCR1/CCR5 pathways, despite increased CCR5 cells in infected mice.

Area of Science:

  • Immunology
  • Neuroscience
  • Infectious Diseases

Background:

  • Encephalitis is a rare complication of acute Trypanosoma cruzi infection.
  • The central nervous system (CNS) is a primary site for Trypanosoma cruzi reactivation in immunocompromised individuals.

Purpose of the Study:

  • To investigate the role of chemokine receptors, specifically CCR5, in T. cruzi-induced meningoencephalitis.
  • To determine if CCR1/CCR5 pathways mediate inflammation during acute T. cruzi infection.

Main Methods:

  • Analyzing gene expression of CCL3/MIP-1alpha and CCL5/RANTES in the CNS of infected mice.
  • Quantifying CCR5-bearing cells in peripheral blood mononuclear cells (PBMC) of infected mice.
  • Assessing the effect of the CCR1/CCR5 antagonist Met-RANTES on PBMC migration in vitro and on CNS inflammation and parasitism in vivo.

Main Results:

  • Acute T. cruzi infection induced CD8-enriched meningoencephalitis with parallel in situ expression of CCL3/MIP-1alpha and CCL5/RANTES mRNA.
  • Increased frequency of CCR5-bearing cells was observed in PBMCs from infected mice.
  • In vitro, Met-RANTES partially inhibited CCL5/RANTES-driven PBMC migration, but in vivo treatment did not alter parasitism or CNS inflammation.

Conclusions:

  • T. cruzi-elicited meningoencephalitis in acute infection is independent of CCR1/CCR5 signaling.
  • While CCR5-bearing cells increase and chemokines are expressed, these pathways do not drive the observed CNS inflammation in this model.

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