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

Abstract

Encephalitis rarely occurs during acute Trypanosoma cruzi infection. However, the central nervous system (CNS) is the major site of infection reactivation in immunocompromised patients. We show that the acute T. cruzi-triggered CD8-enriched meningoencephalitis paralleled the in situ expression of CCL3/MIP-1alpha and CCL5/RANTES mRNA. The frequency of CCR5-bearing cells was increased among peripheral blood mononuclear cells (PBMC) of infected mice. Further, CCL5/RANTES-driven in vitro PBMC migration was partially abrogated by the CCR1/CCR5 antagonist Met-RANTES. However, Met-RANTES treatment of infected mice altered neither parasitism nor intensity and nature of the CNS inflammation, indicating that T. cruzi-elicited meningoencephalitis is a CCR1/CCR5 independent process.

• Authors: Andréa Alice Silva, Ester Roffê, Helton Santiago, Ana Paula Marino, Karina Kroll-Palhares, Mauro Martins Teixeira, Ricardo Tostes Gazzinelli, Joseli Lannes-Vieira
• Journal: Journal of neuroimmunology (J Neuroimmunol) Vol. 184 Issue 1-2 Pg. 156-63 (Mar 2007) ISSN: 0165-5728 [Print] Netherlands
• PMID: 17275101 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• CD8 Antigens
• Ccr1 protein, mouse
• Chemokine CCL5
• Enzyme Inhibitors
• RANTES, Met-
• Receptors, CCR1
• Receptors, CCR5
• Receptors, Chemokine

Topics

• Animals
• CD8 Antigens (metabolism)
• Cell Movement (drug effects)
• Chemokine CCL5 (analogs & derivatives, pharmacology)
• Enzyme Inhibitors (pharmacology)
• Female
• Gene Expression
• Immunohistochemistry
• Inflammation (drug therapy, etiology)
• Meningoencephalitis (complications, drug therapy, etiology, metabolism)
• Mice
• Mice, Inbred C3H
• Mice, Inbred C57BL
• Receptors, CCR1
• Receptors, CCR5 (physiology)
• Receptors, Chemokine (physiology)
• Trypanosoma cruzi (pathogenicity)