Abstract
We evaluated the influence of metabolic syndrome (MS) on acute Trypanosoma cruzi infection. Obese Swiss mice, 70 days of age, were subjected to intraperitoneal infection with 5 × 102 trypomastigotes of the Y strain. Cardiovascular, oxidative, inflammatory, and metabolic parameters were evaluated in infected and non-infected mice. We observed higher parasitaemia in the infected obese group (IOG) than in the infected control group (ICG) 13 and 15 days post-infection. All IOG animals died by 19 days post-infection (dpi), whereas 87.5% of the ICG survived to 30 days. Increased plasma nitrite levels in adipose tissue and the aorta were observed in the IOG. Higher INF-γ and MCP-1 concentrations and lower IL-10 concentrations were observed in the IOG compared to those in the ICG. Decreased insulin sensitivity was observed in obese animals, which was accentuated after infection. Higher parasitic loads were found in adipose and hepatic tissue, and increases in oxidative stress in cardiac, hepatic, and adipose tissues were characteristics of the IOG group. Thus, MS exacerbates experimental Chagas disease, resulting in greater damage and decreased survival in infected animals, and might be a warning sign that MS can influence other pathologies.
Highlights
We evaluated the influence of metabolic syndrome (MS) on acute Trypanosoma cruzi infection
The animals in the control group weighed more during the whole period of evaluation, and only on the 70th day of age, no statistical difference was found between the body masses of control group (CG) and obese group (OG) mice, (Supplementary Data)
From day 40, a higher mean arterial pressure (MAP) was found in the OG when compared to that in the CG, which persisted until the 70th day of age
Summary
We evaluated the influence of metabolic syndrome (MS) on acute Trypanosoma cruzi infection. There has been a significant change in the life habits of the Latin population, a region considered endemic for T. cruzi infection, mainly involving a shift from traditional eating habits to a more westernised diet richer in fat and sugar. Due to this behaviour, the prevalence of obesity and MS in this population has been growing[14]. It is necessary to understand the effects of the interaction between MS and CD, especially since T. cruzi can infect host adipocytes, which can result in changes to their normal function and possibly altering the parasitaemia, tissue parasitic load, and cardiac pathology[15,16,17,18]. It is possible that in the acute phase of T. cruzi infection, MS might exacerbate the deleterious effects of experimental CD
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