Beta2 adrenergic receptor–mediated abnormal myelopoiesis drives neuroinflammation in aged patients with traumatic brain injury

• DOI: 10.1126/sciadv.adp5239
• Publication Date: 2024-07-19T17:59:03Z
• Authors: Rui Jiang; Zhichao Lu; Chenxing Wang; Jun Xiao; Qianqian Liu; Xide Xu; Jinlong Shi; Jianhong Shen; Xingjia Zhu; Peipei Gong; Qian-Xing Zhuang; Kaibin Shi; Wei Shi
• Keywords: Myelopoiesis

Aged patients often suffer poorer neurological recovery than younger after traumatic brain injury (TBI), but the mechanisms underlying this difference remain unclear. Here, we demonstrate abnormal myelopoiesis characterized by increased neutrophil and classical monocyte output impaired nonclassical patrolling population in aged with TBI as well an murine model. Retrograde anterograde nerve tracing indicated that adrenergic input through central amygdaloid nucleus–bone marrow axis drives a β2-adrenergic receptor–dependent manner, which is notably enhanced mice injury. Selective blockade of receptors rebalances improves outcomes TBI. We therefore input-driven exacerbates post-TBI neuroinflammation aged, representing mechanism receptor potential approach to promote