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

dc.contributor.authorSouza, Débora Maria Soares de
dc.contributor.authorCosta, Guilherme de Paula
dc.contributor.authorLeite, Ana Luísa Junqueira
dc.contributor.authorOliveira, Daniela Silva de
dc.contributor.authorPinto, Kelerson Mauro de Castro
dc.contributor.authorFarias, Sílvia Elvira Barros
dc.contributor.authorSimões, Natália Figueira
dc.contributor.authorPaiva, Nívia Carolina Nogueira de
dc.contributor.authorVieira, Paula Melo de Abreu
dc.contributor.authorSilva, Camilo Adalton Mariano da
dc.contributor.authorFigueiredo, Vivian Paulino
dc.contributor.authorMenezes, Ana Paula de Jesus
dc.contributor.authorSilva, André Talvani Pedrosa da
dc.date.accessioned2021-08-31T17:23:27Z
dc.date.available2021-08-31T17:23:27Z
dc.date.issued2020pt_BR
dc.description.abstractThe 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 (n = 10) were infected with 5 × 103 cells 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.pt_BR
dc.identifier.citationSOUZA, D. M. S. de et al. A high-fat diet exacerbates the course of experimental Trypanosoma cruzi infection that can be mitigated by treatment with Simvastatin. Biomed Research International, v. 2020, article ID 1230461, jun. 2020. Disponível em: <https://www.hindawi.com/journals/bmri/2020/1230461/>. Acesso em: 10 jun. 2021.pt_BR
dc.identifier.doihttps://doi.org/10.1155/2020/1230461pt_BR
dc.identifier.issn2314-6141
dc.identifier.urihttp://www.repositorio.ufop.br/jspui/handle/123456789/13620
dc.language.isoen_USpt_BR
dc.rightsabertopt_BR
dc.rights.licenseThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fonte: o PDF do artigo.pt_BR
dc.titleA high-fat diet exacerbates the course of experimental Trypanosoma cruzi infection that can be mitigated by treatment with Simvastatin.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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