| First Author | Tsuchiya M | Year | 2018 |
| Journal | Cell Rep | Volume | 23 |
| Issue | 8 | Pages | 2354-2364 |
| PubMed ID | 29791847 | Mgi Jnum | J:271192 |
| Mgi Id | MGI:6278863 | Doi | 10.1016/j.celrep.2018.04.067 |
| Citation | Tsuchiya M, et al. (2018) Neutrophils Provide a Favorable IL-1-Mediated Immunometabolic Niche that Primes GLUT4 Translocation and Performance in Skeletal Muscles. Cell Rep 23(8):2354-2364 |
| abstractText | 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-1beta, which supports muscle performance through priming exercise-dependent GLUT4 translocation. Thus, during exercise, both IL-1alpha/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. |
