Department of Parasitology and Tropical Medicine, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
Department of Parasitology and Tropical Medicine, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea; Department of Sport Science, Pusan National University, 46241 Busan, Republic of Korea.
Int J Parasitol. 2021 Jan;51(1):63-71. doi: 10.1016/j.ijpara.2020.07.012. Epub 2020 Sep 20.
Obesity is an increasingly prevalent disease worldwide, and genetic and environmental factors are known to regulate the development of obesity and associated metabolic diseases. Emerging studies indicate that innate and adaptive immune cell responses in adipose tissue play critical roles in the regulation of metabolic homeostasis. Parasitic helminths are the strongest natural inducers of type 2 inflammatory responses, and several studies have revealed that helminth infections inversely correlate with metabolic syndrome. Hence, this study investigated whether helminth infections could have preventative effects on high fat diet-induced obesity. Female C57BL/6 mice were maintained on either a low fat diet (LFD, 10% fat) or a high fat diet (HFD, 60% fat) for 6 weeks after Trichinella spiralis infection. The mice were randomly divided into four groups and were fed a normal diet, LFD, LFD after T. spiralis infection (Inf + LFD), a high fat diet (HFD), or HFD after T. spiralis infection (HFD + inf). All groups were assayed for body weight, food efficiency ratio (FER), total body weight gain (g)/total food intake amount (g) fat weight, and blood biochemical parameters. Our data indicate that the HFD + inf group significantly reduced body weight gain, fat mass, total cholesterol, and FER. Analysis of immune cell composition by flow cytometry revealed that T. spiralis promoted strong decreases in proinflammatory adipose macrophages (F4/80CD11c) and T cells. The alterations in microbiota from fecal samples of mice were analyzed, which showed that T. spiralis infection decreased the ratio of Firmicutes to Bacteriodetes, thereby restoring the previously increased ratio of Firmicutes to Bacteriodetes in HFD-fed mice. Moreover, elimination of T. spiralis retained the protective effects in the HFD-fed obese mice whereas flubendazole (FLBZ) treatment increased levels of the families Lachnospiraceae and Ruminococcaceae. In summary, we provided novel data suggesting that helminth infection protects against obesity and the protection was closely related to M2 macrophage proliferation, an inhibiting proinflammatory response. In addition, it alters the microbiota in the gut.
肥胖是一种在全球范围内日益普遍的疾病，已知遗传和环境因素可调节肥胖症和相关代谢疾病的发展。新兴研究表明，脂肪组织中先天和适应性免疫细胞的反应在调节代谢稳态方面起着关键作用。寄生虫蠕虫是最强的 2 型炎症反应天然诱导剂，有几项研究表明，蠕虫感染与代谢综合征呈负相关。因此，本研究探讨了蠕虫感染是否对高脂肪饮食诱导的肥胖具有预防作用。雌性 C57BL/6 小鼠在旋毛虫感染后分别维持在低脂肪饮食（LFD，10%脂肪）或高脂肪饮食（HFD，60%脂肪）6 周。将小鼠随机分为四组，分别给予正常饮食、LFD、LFD 后旋毛虫感染（Inf+LFD）、高脂肪饮食（HFD）或 HFD 后旋毛虫感染（HFD+inf）。所有组均进行体重、食物效率比（FER）、总体重增加（g）/总食物摄入量（g）脂肪重量和血液生化参数检测。我们的数据表明，HFD+inf 组体重增加、脂肪质量、总胆固醇和 FER 显著降低。通过流式细胞术分析免疫细胞组成表明，旋毛虫促进了促炎脂肪巨噬细胞（F4/80CD11c）和 T 细胞的强烈减少。分析来自小鼠粪便样本的微生物群，结果表明旋毛虫感染降低了厚壁菌门与拟杆菌门的比例，从而恢复了高脂肪饮食喂养小鼠中先前增加的厚壁菌门与拟杆菌门的比例。此外，消除旋毛虫保留了对高脂肪饮食喂养肥胖小鼠的保护作用，而氟苯达唑（FLBZ）治疗增加了lachnospiraceae 和 ruminococcaceae 家族的水平。总之，我们提供了新的数据表明，蠕虫感染可预防肥胖，保护作用与 M2 巨噬细胞增殖密切相关，抑制促炎反应。此外，它还改变了肠道中的微生物群。
