Vasoactive intestinal peptide reduces the inflammatory profile in mice infected with Trypanosoma cruzi
| Autor: | Marina Barcelos de Miranda, Dario Elias Pereira, Ivo Santana Caldas, Cristiane Alves da Silva Menezes, Katiane de Oliveira Pinto Coelho Nogueira, Ana Paula Lucas Mota, Priscila Fagundes Mendes, Sandra Aparecida de Lima Moura, Pulchéria Maria Silva Higyno |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Chagas disease
Chagas Cardiomyopathy Chemokine Vasoactive intestinal peptide Neuroimmunomodulation Trypanosoma cruzi Immunology Anti-Inflammatory Agents Parasitemia Trypanosoma brucei Mice Immune system parasitic diseases medicine Animals Chagas Disease Innate immune system biology Myocardium General Medicine medicine.disease biology.organism_classification Mice Inbred C57BL Infectious Diseases Neuroprotective Agents biology.protein Cytokines Parasitology Female Chemokines hormones hormone substitutes and hormone antagonists Vasoactive Intestinal Peptide |
| Zdroj: | Repositório Institucional da UFOP Universidade Federal de Ouro Preto (UFOP) instacron:UFOP |
| ISSN: | 1090-2449 |
| Popis: | Vasoactive intestinal peptide (VIP) has gained great prominence because of its therapeutic potential, which is ascribed to its ability to regulate innate immunity, inhibit antigen-specific Th1 cell responses, and generate T regulatory cells. Additionally, VIP may act as a natural antimicrobial peptide, killing bacteria, fungi, and infective forms of Trypanosoma brucei. Despite the possible relevance of VIP during the course of Chagas disease, studies regarding this in human and experimental Trypanosoma cruzi infections remain poorly characterized. In this work, we evaluated the effects of VIP on systemic and cardiac immune responses during experimental acute infection. C57BL/6 mice were infected with 5000 trypomastigotes of the VL-10 strain of T. cruzi and treated with intraperitoneal VIP injection every other day for one month. After 30 days, we observed no reduction in parasitemia levels. However, we observed a reduction in serum levels of IFN-gamma and IL-2 and an increase in that of IL-4. These data suggest that VIP treatment modified immune responses to favor the Th2 response, which had no impact on parasitemia levels although the serum level of IFN-gamma was reduced. However, this change in immune balance reduced heart damage, as noted by the smaller cardiac volume and the moderate inflammatory infiltrate observed in VIP-treated mice. Our results indicate that VIP treatment reduced the inflammatory response at the cardiac site of mice that were experimentally infected with T. cruzi. These data suggest a protective role for VIP in the heart of infected mice. |
| Databáze: | OpenAIRE |
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