Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 777, Issue -, Pages 26-32Publisher
ELSEVIER
DOI: 10.1016/j.ejphar.2016.02.058
Keywords
AT-RvD1; Chagas disease; T. cruzi antigens; PBMC
Categories
Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [475349/2010-5]
- Fundacao de Apoio a Pesquisa do Estado de Minas Gerais (FAPEMIG) [01/11 CDS APQ 01631/11, CDS APQ 01873-14]
- Rede de Pesquisa em Doencas Infecciosas Humanas e Animais do Estado de Minas Gerais
- Universidade Federal do Triangulo Mineiro (UFTM), Brazil
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Chagas disease is caused by Trypanosoma cruzi (T. cruzi). In some patients with Chagas disease, symptoms progress to chronic chagasic cardiomyopathy. Endogenously, inflammation is resolved in the presence of lipid mediators such as aspirin-triggered RvD1 (AT-RvD1) which has anti-inflammatory and pro-resolution effects. Here, we demonstrated, for the first time, the effects of AT-RvD1 on T. cruzi antigen stimulated peripheral blood mononuclear cells (PBMCs) from patients with Chagas heart disease. The levels of IFN-gamma, THF-alpha, IL-10, and IL-13 increased in PBMCs from cardiac-form Chagas patients in stage B1 (patients with fewer heart abnormalities) stimulated with T. cruzi antigen compared to those in non stimulated PBMCs. AT-RvD1 reduced the IFN-gamma concentrations in PBMCs from patients with Chagas disease stimulated with T. cruzi antigen compared to stimulated with T. cruzi antigen cells. AT-RvD1 treatment resulted in no observable changes in THF-alpha, IL-10, and IL-13 levels. AT-RvD1 significantly decreased the percentage of necrotic cells and caused a significant reduction in the proliferation rate of T. cruzi antigen-stimulated PBMCs from patients with Chagas disease. These findings demonstrate that AT-RvD1 modulates the immune response in Chagas disease patients and might have potential to be used as an alternative approach for slowing the development of further heart damage. (C) 2016 Elsevier B.V. All rights reserved.
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