期刊
FASEB JOURNAL
卷 33, 期 11, 页码 11821-11835出版社
WILEY
DOI: 10.1096/fj.201900477RR
关键词
IL-1 beta inflammasome; metabolic disorder; fatty acid
资金
- Japan Society for the Promotion of Science (JSPS Kakenhi) [JP16K19532, JP15K08527]
- Presto, Japan Science and Technology Agency (JST)
- Hokuriku Life Science Cluster, Ministry of Education, Culture, Sports, Science and Technology (MEXT) Regional Innovation Strategy Support Program
- Takeda Science Foundation
- First Bank of Toyama Scholarship Foundation
- Tokyo Biochemical Research Foundation
Chronic activation of the IL-1 beta system in adipose tissue on metabolic disorders is well demonstrated. However, a mechanism for its expression and activation in the tissue has remained unexplored. Here, we demonstrate that IL-1 beta transcript was enriched in neutrophils of white adipose tissue (WAT) from lean mice. Mechanistically, the interaction of neutrophils with adipocytes induced IL-1 beta expression via NF-kappa B pathway. Lipolysis of adipocytes accumulated neutrophils prior to macrophages in WAT and produced high levels of IL-1 beta via an inflammasome pathway. Leukotriene B-4 (LTB4) production in WAT also contributed to neutrophil accumulation. Furthermore, an LTB4-inflammasome axis contributed to the expression of chemotactic molecules involved in high-fat diet-induced macrophage infiltration into WAT. We have identified previously unappreciated roles for neutrophils in the development of adipose tissue inflammation: robust IL-1 beta production and infiltration of macrophages to initiate chronic inflammation.
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