| Autor: |
Serrano IM; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil.; Advanced Health Public Laboratory, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil., Ribeiro G; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil.; Integrated Translational Program in Chagas Disease, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil., Santos RS; Faculty of Medicine, Federal University of Bahia, Salvador, Brazil., Cruz JS; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil., Lanza FC; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil., Santos EFD; Advanced Health Public Laboratory, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil., Almeida MC; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil., Soares JFS; Faculty of Medicine, Federal University of Bahia, Salvador, Brazil., Luquetti AO; Chagas Disease Study Center, University Hospital, Federal University of Goiás, Goiânia, Brazil., Celedon PAF; Laboratory of Molecular and Systems Biology of Trypanosomatids, Carlos Chagas Institute, Oswaldo Cruz Foundation-Paraná, Curitiba, Brazil., Zanchin NIT; Integrated Translational Program in Chagas Disease, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.; Laboratory of Structural Biology and Protein Engineering Laboratory, Carlos Chagas Institute, Oswaldo Cruz Foundation-Paraná, Curitiba, Brazil., Santos FLN; Advanced Health Public Laboratory, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil.; Integrated Translational Program in Chagas Disease, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil., Reis MGD; Laboratory of Pathology and Molecular Biology, Gonçalo Moniz Institute, Oswaldo Cruz Foundation-Bahia, Salvador, Brazil.; Integrated Translational Program in Chagas Disease, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.; Faculty of Medicine, Federal University of Bahia, Salvador, Brazil.; Department of Epidemiology of Microbial Diseases, Yale School of Public Health, Yale University, New Haven, Connecticut. |
| Abstrakt: |
Chagas disease (CD) is caused by the protozoan Trypanosoma cruzi, which leads to a spectrum of clinical presentations that range from asymptomatic to severe cardiac involvement. The host immune response plays a pivotal role in disease progression. Ig isotypes may contribute to disease pathogenesis. Investigating these components can provide insights into the immunopathogenic mechanisms underlying CD. This cross-sectional study aims to establish a correlation between the Ig profile of individuals infected with T. cruzi with the clinical forms of chronic CD. Serum samples were collected from partner institutions in different states of Brazil. Individuals diagnosed with chronic CD were categorized based on the clinical form of the disease. The indirect ELISA method using the recombinant chimeric Molecular Biology Institute of Paraná membrane protein 8.4 as the antigen was used to determine the Ig profile, including total IgG, IgG1, IgG2, IgG3, and IgG4. Ninety-seven serum samples from patients classified as negative (NEG, n = 38), indeterminate (IND, n = 24), mild cardiac (MC, n = 20), and severe cardiac (SC, n = 15) forms were analyzed. IgG1 exhibited greater levels compared with the other isotypes, showing a significant difference between the MC and IND groups. IgG3 levels were greater in individuals from the MC group compared with the SC group. IgG1 and IgG3 isotypes can serve as biomarkers to evaluate the progression of CD because they exhibit variations across clinical groups. Additional longitudinal studies are necessary to explore the relationship between antibody kinetics and the development of tissue damage. |
