Autor(es): Lima, Luciane Mota ; Cardoso, Luciana Santos ; Santos, Silvane Braga ; Oliveira, Ricardo Riccio ; Oliveira, Sérgio Costa ; Góes, Alfredo Miranda ; Loukas, Alex ; Araujo, Maria Ilma
Data: 2017
Origem: Oasisbr
Assunto(s): HTLV-1; Schistosoma; Proteínas; CXCL9; CXCL10; HTLV-1; Schistosoma proteins; CXCL9; CXCL10
FundingCNPQ (Universal 479417/2008 3), NIH (R01AI079238A).
Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil
Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil / Universidade Federal da Bahia. Faculdade de Farmácia. Departamento de Análises Clínicas e Toxicológicas. Salvador, BA, Brasil / Instituto Nacional de Ciência e Tecnologia em Doenças Tropicais. INCT-DT. CNPq/MCT. Salvador, BA, Brasil
Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil
Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil
Australian Institute of Tropical Health and Medicine, James Cook University, Queensland, Australia
Hospital Universitário Professor Edgard Santos. Serviço de Imunologia. Salvador, BA, Brasil / Escola Baiana de Medicina e Saúde Pública, Salvador, BA, Brasil / Instituto Nacional de Ciência e Tecnologia em Doenças Tropicais. INCT-DT. CNPq/MCT. Salvador, BA, Brasil
HTLV-1 is the causal agent of Adult T cell Leukemia/lymphoma (ATLL) and HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). The immune response to HTLV-1-infection is polarized to the Th1-type, and the presence of CXCL9/CXCL10 chemokines may lead to an increase in the recruitment of pro-inflammatory molecules in spinal cord tissue, contributing to the damage observed in the development of HAM/TSP. It has been observed that in chronic helminth-infections, such as schistosomiasis, there is a deviation toward the Th2/regulatory immune response. Objective: To evaluate the ability of Schistosoma spp. proteins to decrease the in vitro CXCL9 and CXCL10 production by PBMC of HTLV-1-infected individuals. Methods: The Schistosoma proteins rSm29, rSh-TSP-2 and PIII were added to PBMC cultures of HTLV-1- infected individuals and the levels of chemokines in the supernatants were measured using a sandwich ELISA method. Results: The addition of rSm29 to the cultures resulted in decreased production of CXCL9 in all the analyzed individuals and HAM/TSP group (18167 ± 9727 pg/mL, p = 0.044; 20237 ± 6023 pg/mL, p = 0.028, respectively) compared to the levels in unstimulated cultures (19745 ± 9729 pg/mL; 25078 ± 2392 pg/mL, respectively). The addition of rSh-TSP-2 decreased the production of CXCL9 in all studied individuals and carriers group (16136 ± 9233 pg/mL, p = 0.031; 13977 ± 8857 pg/mL, p = 0.026) vs unstimulated cultures (19745 ± 9729 pg/mL; 18121 ± 10508 pg/mL, respectively). Addition of PIII did not alter the results. There was no significant change in the levels of CXCL10 by the addition of the studied proteins. Conclusion: The Schistosoma proteins used in this study were able to down modulate the production of CXCL9, a chemokine associated with the inflammatory process in HTLV-1-infection.
