Abstract
Sera and peripheral blood mononuclear cells (PBMC) from patients displaying different clinical symptoms as well as from normal uninfected individuals (NI) were used to evaluate the humoral and cellular responses of Chagas' disease patients to Trypanosoma cruzi-derived paraflagellar rod proteins (PFR). Our results show that sera from both asymptomatic Chagas' disease patients (ACP) and cardiac Chagas' disease patients (CCP) have higher levels of antibodies to PFR than sera from NI. Immunoglobulin G1 (IgG1) and IgG3 were the main Ig isotypes that recognized PFR. We also tested three recombinant forms of PFR, named rPAR-1, rPAR-2, and rPAR-3, by Western blot analysis. Sera from seven out of eight patients with Chagas' disease recognized one of the three rPAR forms. Sera from 75, 50, and 37.5% of Chagas' disease patients tested recognized rPAR-3, rPAR-2, and rPAR-1, respectively. PFR induced proliferation of 100 and 70% of PBMC from ACP and CCP, respectively. Further, stimulation of cells from Chagas' disease patients with PFR enhanced the frequencies of both small and large CD4(+) CD25(+) and CD4(+) CD69(+) lymphocytes, as well as that of small CD8(+) CD25(+) lymphocytes. Finally, we evaluated the ability of PFR to elicit the production of gamma interferon (IFN-gamma) by PBMC from patients with Chagas' disease. Fifty percent of the PBMC from ACP as well as CCP produced IFN-gamma upon stimulation with PFR. PFR enhanced the percentages of IFN-gamma-producing cells in both CD3(+) and CD3(-) populations. Within the T-cell population, large CD4(+) T lymphocytes were the main source of IFN-gamma.
Highlights
Chagas’ disease, caused by infection with the protozoan parasite Trypanosoma cruzi, is a major public health problem in Latin America
Our results show that sera from both asymptomatic Chagas’ disease patients (ACP) and cardiac Chagas’ disease patients (CCP) have higher levels of antibodies to PFR than sera from normal uninfected individuals (NI)
Our results show that the majority of the patients with Chagas’ disease (80%) yielded positive results when we employed PFR in an enzyme-linked immunosorbent assay (ELISA)
Summary
Chagas’ disease, caused by infection with the protozoan parasite Trypanosoma cruzi, is a major public health problem in Latin America. 20 million people are infected, and an additional 100 million individuals are at risk of infection Reductions in these numbers are expected, since major advances in control of the insect vectors and in methods for screening blood banks have been made, resulting in substantial decreases in frequencies of T. cruzi transmission in several countries of South America [28, 33, 34]. PFR in humans by accessing both humoral and cellular responses of clinically defined Chagas’ disease patients, naturally infected with T. cruzi. Our results show that the majority of patients with Chagas’ disease develop both humoral and cellular responses to PFR, with dominant responses for PAR-2 and PAR-3
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