Intestinal helminthes induce immunosuppressive responses as well as type 2 immunity. Their suppressive properties are intended to regulate inflammatory diseases such as allergies and autoimmune diseases. This study evaluated whether helminthic infections suppress obesity, a chronic inflammatory state, using an intestinal nematode, Heligmosomoides polygyrus (Hp). Infection with Hp at the same time as feeding a high‐fat diet (HFD) prevented weight gain, dyslipidaemia and glucose intolerance observed in uninfected obese mice. Immunologically, Hp infection skewed M1 macrophages to M2 macrophages and induced type 2 innate lymphoid cells in adipose tissues. The expression of interleukin (IL)‐33, a potent initiator of type 2 responses, was also increased in association with uncoupled protein 1 (UCP1). To further investigate the anti‐obesity effects of IL‐33 in mice infected with Hp, IL‐33‐deficient mice were fed the HFD and infected with Hp. These mutant mice rapidly gained weight compared with wild‐type mice, indicating the anti‐obesity effect of IL‐33. In the absence of IL‐33, the rapid increase in weight was not prevented, and type 2 responses and UCP1 expression were not observed even during Hp infection. These results suggested that the suppression of obesity by Hp is dependent on IL‐33.

中文翻译：

---

IL-33对预防高脂饮食引起的肥胖的肠道蠕虫小鼠至关重要。

肠蠕虫诱导免疫抑制反应以及2型免疫。它们的抑制特性旨在调节炎症性疾病，例如过敏和自身免疫性疾病。这项研究使用肠线虫Heligmosomoides polygyrus评估了蠕虫感染是否抑制肥胖（一种慢性炎症状态）（生命值）。在未感染的肥胖小鼠中，与高脂饮食（HFD）喂养同时感染Hp可防止体重增加，血脂异常和葡萄糖耐量异常。免疫学上，Hp感染使M1巨噬细胞偏向M2巨噬细胞，并诱导了脂肪组织中的2型先天淋巴样细胞。白细胞介素（IL）-33（一种有效的2型应答启动子）的表达也随着未偶联蛋白1（UCP1）的表达而增加。为了进一步研究IL-33在感染Hp的小鼠中的抗肥胖作用，向IL-33缺陷的小鼠喂食了HFD并感染了Hp。与野生型小鼠相比，这些突变型小鼠体重迅速增加，表明IL-33具有抗肥胖作用。在没有IL-33的情况下，体重的迅速增加是无法避免的，即使在Hp感染期间也未观察到2型应答和UCP1表达。这些结果表明，Hp对肥胖的抑制作用取决于IL-33。