Neutrophils Provide a Favorable IL-1-Mediated Immunometabolic Niche that Primes GLUT4 Translocation and Performance in Skeletal Muscles

摘要: Metabolic immunomodulation involving IL-1 has been investigated for unfavorable metabolic effects, including obesity, but a potentially favorable role remains unclear. Here, we find mechanistic interactions between working skeletal muscles and locally recruited neutrophils expressing IL-1β, which supports muscle performance through priming exercise-dependent GLUT4 translocation. Thus, during exercise, both IL-1α/β-deficient neutrophil-depleted mice similarly exhibit increased fatigability associated with impaired glucose homeostasis due to dysregulation. Deficiency of IL-1-producing results in intrinsic abnormalities represented by aberrant Rac1 signaling irregular GLUT4-storage vesicles, suggesting that these properties are maintained local produced upon possibly on daily basis. We propose highly engaged via regulation, coordinates inflammatory microenvironments supporting metabolism.