 Traumatic brain injury, TBI, accelerates fracture healing, but the underlying mechanism remains unclear. Evidence suggests that the central nervous system, CNS, plays a key role in regulating immune system and skeletal homeostasis. However, the impact of CNS injury on hematopoiesis commitment has been overlooked. We found that the dramatically increased sympathetic tone associated with TBI accelerated fracture healing, chemical sympathectomy blocks TBI-induced fracture healing. TBI-induced hypersensitivity of adrenergic signaling promotes the proliferation of bone marrow hematopoietic stem cells, HSCs, and swiftly skews HSCs towards anti-inflammatory myeloid cells within 14 days, which favours fracture healing. Knockout of beta-3 or beta-2 adrenergic receptors, arse, eliminates TBI-mediated anti-information macrophage expansion and TBI-accelerated fracture healing. Eye-in-a-sequencing of bone marrow. This article was authored by Wei-jen Liu, Wei-jen, Mao Xia, and others. We are article.tv, links in the description below.