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

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2023-09-15 DOI:10.1016/j.imbio.2023.152747

Amanda Goulart , Naira Ferreira Anchieta , Pedro Alexandre Sampaio , Vânia Brazão , Jefferson Luiz Da Silva , Gisele Bulhões Portapilla , Andressa Duarte , Daiane Yukie Tezuca , Maiara Voltarelli Providello , Angelita Maria Stabile , José Clóvis do Prado Júnior

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引用次数: 0

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.

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自助餐厅饮食诱导的肥胖重塑了急性克氏锥虫感染的免疫反应。

背景：肥胖是一个全球性问题，与多种疾病有关，包括高血压、糖尿病、关节炎和心血管疾病。近年来，随着肥胖患病率的增加，主要是在发展中国家，研究肥胖对各种疾病的影响很重要，包括由原生动物克氏锥虫引起的恰加斯病等传染病。考虑到富含盐、糖和脂肪的饮食与肥胖有关，本研究旨在评估自助餐厅饮食（CAF）诱导的肥胖对克鲁兹霉感染大鼠免疫反应的影响。方法：雄性Wistar Hannover大鼠随意饮水和进食（食物组）。CAF喂养组接受正常啮齿动物饮食或CAF。用105种锥虫体形式的克鲁兹锥虫Y株腹膜内感染动物，该Y株存在于先前感染的小鼠的全血中。结果：与喂食食物的大鼠相比，喂食CAF的大鼠内脏脂肪组织重量显著增加。与非肥胖感染大鼠相比，在肥胖感染的大鼠中观察到CD3+CD4+辅助性脾脏T细胞以及CD11b和巨噬细胞的显著减少。此外，与对照动物相比，肥胖动物的巨噬细胞显示出RT1b水平降低。此外，与肥胖感染大鼠相比，巨噬细胞活化的重要因素INF-γ减少。结论：这些结果表明CAF可以削弱细胞介导的对克鲁兹锥虫的免疫反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464