IL-33 is essential to prevent high fat diet-induced obesity in mice infected with an intestinal helminth.
IL-33 is essential to prevent high fat diet-induced obesity in mice infected with an intestinal helminth.
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DOI：
10.1111/pim.12700
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发表时间：
2020-02
影响因子：
2.2
通讯作者：
Seiji Obi;C. Shimokawa;Mizuki Katsuura;A. Olia;T. Imai;K. Suzue;H. Hisaeda
中科院分区：
文献类型：
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作者：
Seiji Obi;C. Shimokawa;Mizuki Katsuura;A. Olia;T. Imai;K. Suzue;H. Hisaeda
肠道蠕虫可诱导免疫抑制反应和2型免疫。它们的抑制特性旨在调节炎症性疾病，如过敏和自身免疫性疾病。这项研究使用肠道线虫多回螺旋体(HP)来评估蠕虫感染是否能抑制肥胖，这是一种慢性炎症状态。在喂食高脂饮食(HFD)的同时感染幽门螺杆菌可预防未感染肥胖小鼠的体重增加、血脂异常和糖耐量减低。在免疫方面，Hp感染使M1巨噬细胞向M2巨噬细胞倾斜，并诱导脂肪组织中的2型固有淋巴样细胞。与解偶联蛋白1(UCP1)相关的IL-33表达也增加，IL-33是2型反应的有力启动者。为进一步探讨IL-33对幽门螺杆菌感染小鼠的减肥作用，将IL-33基因缺陷小鼠喂饲高脂饲料并感染幽门螺杆菌。与野生型小鼠相比，这些突变小鼠体重迅速增加，表明IL-33具有减肥作用。在没有IL-33的情况下，体重的快速增加没有被阻止，即使在HP感染期间也没有观察到2型反应和UCP1的表达。这些结果提示幽门螺杆菌对肥胖的抑制作用依赖于IL-33。
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, dyslipidemia, 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. 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 wildtype 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.