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 (F4/80⁺CD11c⁺) 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.

肥胖症是世界范围内日益流行的疾病，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，脂肪组织中的先天性和适应性免疫细胞反应在代谢稳态的调节中起着关键作用。寄生蠕虫是 2 型炎症反应的最强天然诱导剂，几项研究表明，蠕虫感染与代谢综合征呈负相关。因此，本研究调查了蠕虫感染是否对高脂肪饮食引起的肥胖具有预防作用。雌性 C57BL/6 小鼠在旋毛虫感染后维持低脂饮食（LFD，10% 脂肪）或高脂肪饮食（HFD，60% 脂肪）6 周感染。将小鼠随机分为四组，分别喂食正常饮食、LFD、螺旋线虫感染后的LFD （Inf + LFD）、高脂肪饮食（HFD）或螺旋线虫感染后的HFD（HFD + inf）。测定所有组的体重、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。我们的数据表明，HFD + inf 组显着降低了体重增加、脂肪量、总胆固醇和 FER。通过流式细胞术对免疫细胞组成的分析表明，螺旋藻促进促炎脂肪巨噬细胞 (F4/80 ⁺ CD11c ⁺) 和 T 细胞。分析了小鼠粪便样本中微生物群的变化，这表明螺旋藻感染降低了厚壁菌门与拟杆菌门的比率，从而恢复了先前在 HFD 喂养的小鼠中增加的厚壁菌门与拟杆菌门的比率。此外，消除旋毛虫保留在HFD喂养的肥胖小鼠的保护作用，而氟苯咪唑（FLBZ）处理提高家庭和毛螺的Ruminococcaceae水平。总之，我们提供了新的数据，表明蠕虫感染可以预防肥胖，并且这种保护与 M2 巨噬细胞增殖密切相关，M2 巨噬细胞增殖是一种抑制促炎反应。此外，它会改变肠道中的微生物群。