4.7 Article

Effects of aspirin-triggered resolvin D1 on peripheral blood mononuclear cells from patients with Chagas' heart disease

期刊

EUROPEAN JOURNAL OF PHARMACOLOGY
卷 777, 期 -, 页码 26-32

出版社

ELSEVIER
DOI: 10.1016/j.ejphar.2016.02.058

关键词

AT-RvD1; Chagas disease; T. cruzi antigens; PBMC

资金

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [475349/2010-5]
  2. Fundacao de Apoio a Pesquisa do Estado de Minas Gerais (FAPEMIG) [01/11 CDS APQ 01631/11, CDS APQ 01873-14]
  3. Rede de Pesquisa em Doencas Infecciosas Humanas e Animais do Estado de Minas Gerais
  4. Universidade Federal do Triangulo Mineiro (UFTM), Brazil

向作者/读者索取更多资源

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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