A high-fat diet exacerbates the course of experimental Trypanosoma cruzi infection that can be mitigated by treatment with simvastatin

• Autor(a) principal: Débora Maria Soares de Souza
• Data de Publicação: 2020
• Outros Autores: Guilherme de Paula Costa, Ana Luísa Junqueira Leite, Daniela Silva de Oliveira, Kelerson Mauro de Castro Pinto, Sílvia Elvira Barros Farias, Natália Figuerôa Simões, Nívia Carolina Nogueira de Paiva, Paula Melo de Abreu Vieira, Camilo Adalton Mariano da Silva, Vivian Paulino Figueiredo, Ana Paula de Jesus Menezes, André Talvani Pedrosa da Silva
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFMG
• Texto Completo: https://doi.org/10.1155/2020/1230461; http://hdl.handle.net/1843/51404; https://orcid.org/0000-0001-8634-8654; https://orcid.org/0000-0002-2048-9400; https://orcid.org/0000-0001-7033-7686; https://orcid.org/0000-0002-5683-9556; https://orcid.org/0000-0002-2834-8864; https://orcid.org/0000-0001-9818-5178; https://orcid.org/0000-0002-6685-6229
• topic: Trypanosoma cruzi; Myocarditis; Simvastatin; High-fat diet; Trypanosoma cruzi; Miocardite; Sinvastatina; Dieta hiperlipídica

The protozoan Trypanosoma cruzi is responsible for triggering a damage immune response in the host cardiovascular system. This parasite has a high affinity for host lipoproteins and uses the low-density lipoprotein (LDL) receptor for its invasion. Assuming that the presence of LDL cholesterol in tissues could facilitate T. cruzi proliferation, dietary composition may affect the parasite-host relationship. Therefore, the aim of this study was to evaluate myocarditis in T. cruzi-infected C57BL/6 mice—acute phase—fed a high-fat diet and treated with simvastatin, a lipid-lowering medication. Animals () were infected with of the VL-10 strain of T. cruzi and treated or untreated daily with 20 mg/kg simvastatin, starting 24 h after infection and fed with a normolipidic or high-fat diet. Also, uninfected mice, treated or not with simvastatin and fed with normolipidic or high-fat diet, were evaluated as control groups. Analyses to measure the production of chemokine (C-C motif) ligand 2 (CCL2), interferon- (IFN-) γ, interleukin- (IL-) 10, and tumor necrosis factor (TNF); total hepatic lipid dosage; cholesterol; and fractions, as well as histopathological analysis, were performed on day 30 using cardiac and fat tissues. Our results showed that the high-fat diet increased (i) parasite replication, (ii) fat accumulation in the liver, (iii) total cholesterol and LDL levels, and (iv) the host inflammatory state through the production of the cytokine TNF. However, simvastatin only reduced the production of CCL2 but not that of other inflammatory mediators or biochemical parameters. Together, our data suggest that the high-fat diet may have worsened the biochemical parameters of the uninfected and T. cruzi-infected animals, as well as favored the survival of circulating parasites.