Neuroinflammation Mediates Faster Brachial Plexus Regeneration in Subjects with Cerebral Injury

Fan SU; Guobao Wang; Tie LI; Su Jiang; Aiping YU; Wendong XU; Fan SU; Guobao Wang; Tie LI; Su Jiang; Aiping YU; Xiaomin Wang; Wendong XU; Fan SU; Tie LI; Wendong XU; Fan SU; Tie LI; Wendong XU; Wendong XU

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Neuroinflammation Mediates Faster Brachial Plexus Regeneration in Subjects with Cerebral Injury

Author: Fan SU ¹ ; Guobao WANG ¹ ; Tie LI ¹ ; Su JIANG ¹ ; Aiping YU ¹ ; Wendong XU ¹ ; Fan SU ² ; Guobao WANG ² ; Tie LI ² ; Su JIANG ² ; Aiping YU ² ; Xiaomin WANG ² ; Wendong XU ² ; Fan SU ³ ; Tie LI ³ ; Wendong XU ³ ; Fan SU ⁴ ; Tie LI ⁴ ; Wendong XU ⁴ ; Wendong XU ⁵
Author Information

1. Department of Hand Surgery, Huashan Hospital, Shanghai Medical College, Fudan University
2. Department of Hand and Upper Extremity Surgery, Jing’an District Central Hospital, Fudan University
3. The National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University
4. Institute of Brain Science, State Key Laboratory of Medical Neurobiology and Collaborative Innovation Center for Brain Science, Fudan University
5. Co-innovation Center of Neuroregeneration, Nantong University
Publication Type:Journal Article
Keywords: Brachial plexus injury; Cerebral injury; Contralateral seventh cervical nerve transfer; Macrophage polarization; Nerve regeneration; Nerve transfer; Neuroinflammation
From: Neuroscience Bulletin 2021;37(11):1542-1554
CountryChina
Language:Chinese
Abstract: Our previous investigation suggested that faster seventh cervical nerve (C7) regeneration occurs in patients with cerebral injury undergoing contralateral C7 transfer. This finding needed further verification, and the mechanism remained largely unknown. Here, Tinel’s test revealed faster C7 regeneration in patients with cerebral injury, which was further confirmed in mice by electrophysiological recordings and histological analysis. Furthermore, we identified an altered systemic inflammatory response that led to the transformation of macrophage polarization as a mechanism underlying the increased nerve regeneration in patients with cerebral injury. In mice, we showed that, as a contributing factor, serum amyloid protein A1 (SAA1) promoted C7 regeneration and interfered with macrophage polarization in vivo. Our results indicate that altered inflammation promotes the regenerative capacity of the C7 nerve by altering macrophage behavior. SAA1 may be a therapeutic target to improve the recovery of injured peripheral nerves.