骨髓生成
神经炎症
创伤性脑损伤
医学
肾上腺素能受体
神经科学
封锁
人口
受体
内科学
内分泌学
心理学
生物
炎症
精神科
造血
细胞生物学
干细胞
环境卫生
作者
Rui Jiang,Zhichao Lu,Chenxing Wang,Jun Xiao,Q. Liu,Xide Xu,Jinlong Shi,Jianhong Shen,Xingjia Zhu,Peipei Gong,Qian‐Xing Zhuang,Kaibin Shi,Wei Shi
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2024-07-19
卷期号:10 (29)
标识
DOI:10.1126/sciadv.adp5239
摘要
Aged patients often suffer poorer neurological recovery than younger patients 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 but impaired nonclassical patrolling monocyte population in aged patients with TBI as well as in an aged murine TBI model. Retrograde and anterograde nerve tracing indicated that increased adrenergic input through the central amygdaloid nucleus–bone marrow axis drives abnormal myelopoiesis after TBI in a β2-adrenergic receptor–dependent manner, which is notably enhanced in aged mice after injury. Selective blockade of β2-adrenergic receptors rebalances abnormal myelopoiesis and improves the outcomes of aged mice after TBI. We therefore demonstrate that increased β2-adrenergic input-driven abnormal myelopoiesis exacerbates post-TBI neuroinflammation in the aged, representing a mechanism underlying the poorer recovery of aged patients and that blockade of β2-adrenergic receptor is a potential approach to promote neurological recovery after TBI.
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