Trypanosoma cruzi: Populations bearing opposite virulence induce differential expansion of circulating CD3+CD4−CD8− T cells and cytokine serum levels in young and adult rats

• Published in: Experimental parasitology 2007-08, Vol.116 (4), p.366-374
• Main Authors: Nagib, Patrícia R.A., Dutra, Walderez O., Chiari, Egler, Machado, Conceição R.S.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; CD3 Complex - blood; Chagas disease; Chagas Disease - immunology; Chagas Disease - parasitology; Cytokines - blood; Double-negative T cells; Fundamental and applied biological sciences. Psychology; IFN-γ; IL-10; Interferon-gamma - blood; Interleukin-10 - blood; Life cycle. Host-agent relationship. Pathogenesis; Male; Protozoa; Rats; Rats, Sprague-Dawley; T-Lymphocytes - immunology; TNF-α; Trypanosoma cruzi; Trypanosoma cruzi - immunology; Trypanosoma cruzi - pathogenicity; Tumor Necrosis Factor-alpha - blood; Virulence - immunology
• ISSN: 0014-4894; 1090-2449
• DOI: 10.1016/j.exppara.2007.02.003

The JG strain is the least virulent while the CL-Brener clone is one of the most virulent Trypanosoma cruzi populations in young rats. In this study, we determined that the parasitemia peak values in CL-Brener clone-infected adult rats were 50-fold lower than in young rats and that mortality was null as compared to 45% death in young rats. Low parasitemia, milder and sustained myocarditis and myositis characterized JG infections. CL-Brener clone caused a significantly higher production of pro-inflammatory cytokines and higher expansion of CD3+CD4−CD8−, double-negative (DN) T cells, during the acute phase in both adult and young rats. DN T cell frequencies correlated with IFN-γ levels. These findings may explain the higher inflammation and fast acute phase resolution in CL-Brener infection. In young rats, IL-10 levels were similar in both infections. The IL-10/IFN-γ ratio was higher in JG acute infection in accordance with the milder inflammation and parasite persistence leading to a chronic phase. In conclusion, virulence and pathogenicity depend on T. cruzi ability to induce expansion of DN T cells and production of specific cytokines.