1. IL‐33 is essential to prevent high‐fat diet–induced obesity in mice infected with an intestinal helminth.
- Author
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Obi, Seiji, Shimokawa, Chikako, Katsuura, Mizuki, Olia, Alex, Imai, Takashi, Suzue, Kazutomo, and Hisaeda, Hajime
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WESTERN diet , *INNATE lymphoid cells , *HELMINTHIASIS , *ADIPOSE tissues , *FAT cells , *MICE - Abstract
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. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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