Abstract：
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: These results indicate that a CAF can impair the cell-mediated immune response against T. cruzi.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: These results indicate that a CAF can impair the cell-mediated immune response against T. cruzi.
摘要：
背景：肥胖是与多种疾病相关的全球性问题，包括高血压,糖尿病,关节炎和心血管疾病。随着近年来肥胖患病率的增加,主要在发展中国家，重要的是研究它对各种疾病的影响，包括传染病,比如查加斯病，由原生动物克氏锥虫引起的。考虑到富含盐的饮食，糖,脂肪与肥胖有关，这项研究旨在评估自助餐饮食（CAF）诱导的肥胖对T.cruzi感染大鼠免疫反应的影响。
方法:雄性Wistar汉诺威大鼠随意提供水和食物(食物组)。饲喂CAF的组接受正常啮齿动物饮食或CAF。用存在于先前感染的小鼠的全血中的105个锥虫T.cruzi的Y菌株的锥虫形式对动物进行腹膜内感染。
结果：与饲喂大鼠相比，饲喂CAF的大鼠内脏脂肪组织重量显着增加。与非肥胖感染大鼠相比，在肥胖感染大鼠中观察到CD3+CD4+辅助脾T细胞显著减少，以及CD11b和巨噬细胞。此外,与对照动物相比，肥胖动物的巨噬细胞显示出降低的RT1b水平。此外，INF-γ,巨噬细胞活化的一个重要因素，与肥胖感染的大鼠相比，肥胖感染的大鼠减少了。
结论：这些结果表明，CAF可以损害细胞介导的针对克氏锥虫的免疫应答。
方法:雄性Wistar汉诺威大鼠随意提供水和食物(食物组)。饲喂CAF的组接受正常啮齿动物饮食或CAF。用存在于先前感染的小鼠的全血中的105个锥虫T.cruzi的Y菌株的锥虫形式对动物进行腹膜内感染。
结果：与饲喂大鼠相比，饲喂CAF的大鼠内脏脂肪组织重量显着增加。与非肥胖感染大鼠相比，在肥胖感染大鼠中观察到CD3+CD4+辅助脾T细胞显著减少，以及CD11b和巨噬细胞。此外,与对照动物相比，肥胖动物的巨噬细胞显示出降低的RT1b水平。此外，INF-γ,巨噬细胞活化的一个重要因素，与肥胖感染的大鼠相比，肥胖感染的大鼠减少了。
结论：这些结果表明，CAF可以损害细胞介导的针对克氏锥虫的免疫应答。
