Cafeteria diet-induced obesity remodels immune response in acute Trypanosoma cruzi infection

•CAF-fed rats showed a increase in adipose tissue and metabolic syndrome related disorders, when compared to chow-fed rats.•Splenic CD3+ CD4+ T cells and macrophages were reduced in obese-infected rats compared to non-obese-infected rats.•INF-γ and RT1b were reduced in obese infected rats.•A CAF can impair the cell-mediated immune response against T. cruzi. Obesity is a global problem associated with several conditions, including hypertension, diabetes, arthritis and cardiovascular diseases. With the increase in the prevalence of obesity in recent years, mostly in developing countries, it is important to study its impact on various diseases, including infectious illnesses, such as Chagas disease, caused by the protozoan Trypanosoma cruzi. Considering that a diet rich in salt, sugar, and fat is associated with obesity, this study aimed to evaluate the influence of cafeteria diet (CAF)-induced obesity on immune responses in T. cruzi-infected rats. Male Wistar Hannover rats were provided with water and food ad libitum (chow group). The CAF-fed groups received a normal rodent diet or CAF. The animals were intraperitoneally infected with 105 trypomastigote forms of the Y strain of T. cruzi present in the whole blood from a previously infected mouse. CAF-fed rats showed a significant increase in visceral adipose tissue weight compared to chow-fed rats. A significant reduction in CD3+ CD4+ helper splenic T cells was observed in obese-infected rats compared to non-obese-infected rats, as well as CD11b and macrophages. In addition, macrophages from obese animals displayed reduced RT1b levels compared to those from control animals. Moreover, INF-γ, an important factor in macrophage activation, was reduced in obese-infected rats compared with their counterparts. These results indicate that a CAF can impair the cell-mediated immune response against T. cruzi.