期刊
CELL REPORTS
卷 23, 期 8, 页码 2354-2364出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.04.067
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资金
- Japan Society for the Promotion of Science [16K11580, 17H02076, 16K12863]
- Grants-in-Aid for Scientific Research [17H02076, 16K11580, 16K12863] Funding Source: KAKEN
Metabolic immunomodulation involving IL-1 has been investigated for unfavorable metabolic effects, including obesity, but a potentially favorable role for IL-1 remains unclear. Here, we find mechanistic interactions between working skeletal muscles and locally recruited neutrophils expressing IL-1 beta, which supports muscle performance through priming exercise-dependent GLUT4 translocation. Thus, during exercise, both IL-1 alpha/beta-deficient and neutrophil-depleted mice similarly exhibit increased fatigability associated with impaired muscle glucose homeostasis due to GLUT4 dysregulation. Deficiency of IL-1-producing neutrophils results in intrinsic abnormalities represented by aberrant Rac1 signaling and irregular GLUT4-storage vesicles, suggesting that these properties are maintained by local IL-1 produced by recruited neutrophils upon exercise, possibly on a daily basis. We propose that neutrophils are highly engaged in skeletal muscle performance via IL-1 regulation, which coordinates favorable inflammatory microenvironments supporting muscle glucose metabolism.
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