PHENOTYPIC ANALYSIS OF MACROPHAGE SUBSETS IN CHAGASIC RATS TREATED WITH GHRELIN

2016 
Trypanosoma cruzi is an intracellular protozoan parasite causing Chagas disease, which affects thousands of people around of world. The treatment remains partially ineffective, involving targeted therapies directed to the parasite. Ghrelin is a peptide hormone and evidences support its role in regulating cell proliferation and immunity. Macrophages are one of the first barriers against intracellular pathogens, producing cytokines and effector molecules. The objective of this study was to evaluate the effects of ghrelin treatment in macrophages during the acute phase of Chagas disease. Twenty male Wistar rats (100-110g) were grouped in: control (C), control/ghrelin supplied (CG), infected (I) and infected/ghrelin supplied (IG). Rats were infected with 2x10 5 trypomastigotes (Y strain) subcutaneously supplied with 100µg of ghrelin/Kg/day during 14 days. Animals were killed on the 15 th day after infection and peritoneal macrophages were collected. Phenotypic analysis of macrophage subsets and macrophage receptors (RT1B + ; MHC class II) was determined by labeling with anti-rat macrophage subset (PE) and anti-rat RT1B (PerCP) monoclonal antibodies (Becton Dickinson). Data were assessed by flow cytometry FACScan and FACSDiva software. Our results showed no difference in macrophage subsets percentage in the IG group when compared to infected group. However, a statistical difference in RT1B + macrophages percentage was observed in IG group when compared to its counterparts. Our data reveal that during Chagas disease a strong innate immune response is mounted, and ghrelin supplementation seems to improve RT1B + macrophages activation during the acute phase of infection, contributing to improve the innate immune response.  KEY WORDS: Chagas disease, ghrelin, macrophages, rat FINANCIAL SUPPORT: Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP - 2014/18682-3); Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES).
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