AIMS Neuroinflammation is one of the most important processes in the pathogenesis of Parkinson's disease (PD). Sensory disturbances are common in patients with PD, but the underlying pathophysiological mechanisms remain unknown. This study aimed to characterize the activation of Schwann cells (SCs) and the increase of expression of inflammatory cytokines IL-1β, IL-6, and TNF-α in the sural nerve of PD, and further explore whether peripheral nerve inflammation is the cause of PD sensory disturbances. METHODS A total of 14 patients with PD (including 5 with sensory disturbances and 9 without sensory disturbances) and 6 controls were included. The excitation and conduction function of sural nerve was detected by sural nerve electrophysiological examination. With sural nerve biopsy samples, ultrastructural changes of sural nerve were observed by electron microscopy; Schwann cell biomarker glial fibrillary acid protein (GFAP) and inflammatory cytokines including interleukin-1beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were detected by immunohistochemistry, and the outcome of immunostaining slice was semiquantitatively counted; double immunofluorescence was used to identify the locus immunoreactive for inflammatory cytokines. RESULTS Compared with healthy controls, nerve conduction velocity (NCV) slowed down and sensory nerve action potential (SNAP) amplitude decreased in PD patients, accompanied by axonal degeneration and demyelinating lesions, and expression of GFAP and inflammatory cytokines was increased. Inflammatory cytokines were significantly colocalized with GFAP and slightly colocalized with NF. These indicators did not differ significantly between PD patients with and without sensory disturbances. CONCLUSION Our study results suggest that peripheral sensory nerve injury exists in PD patients, accompanied by Schwann cell activation and inflammation, thus demonstrate peripheral nerve inflammation participates in the pathophysiological process of PD but it is not necessarily related to the patient's sensory disturbance.

中文翻译：

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患者腓肠神经中激活的雪旺氏细胞和增加的炎性细胞因子 IL-1β、IL-6 和 TNF-α 与帕金森病的特定感觉障碍缺乏密切关系。

AIMS 神经炎症是帕金森病 (PD) 发病机制中最重要的过程之一。感觉障碍在 PD 患者中很常见，但潜在的病理生理机制尚不清楚。本研究旨在表征 PD 腓肠神经中雪旺细胞 (SCs) 的活化和炎性细胞因子 IL-1β、IL-6 和 TNF-α 的表达增加，并进一步探讨周围神经炎症是否是病因PD 感觉障碍。方法共纳入PD患者14例（其中感觉障碍5例，无感觉障碍9例）和对照者6例。腓肠神经电生理检查检测腓肠神经兴奋和传导功能。使用腓肠神经活检样本，电镜观察腓肠神经超微结构改变；免疫组化检测雪旺细胞生物标志物胶质纤维酸性蛋白（GFAP）和炎症细胞因子，包括白介素-1β（IL-1β）、白介素6（IL-6）和肿瘤坏死因子-α（TNF-α），结果免疫染色切片半定量计数；双免疫荧光用于鉴定对炎性细胞因子具有免疫反应性的位点。结果 与健康对照组相比，PD患者神经传导速度（NCV）减慢，感觉神经动作电位（SNAP）波幅降低，伴有轴索变性和脱髓鞘病变，GFAP和炎性细胞因子表达增加。炎性细胞因子与 GFAP 显着共定位，与 NF 轻微共定位。这些指标在有和没有感觉障碍的 PD 患者之间没有显着差异。结论 本研究结果提示PD患者存在周围感觉神经损伤，并伴有雪旺细胞活化和炎症反应，说明周围神经炎症参与了PD的病理生理过程，但与患者感觉障碍不一定有关。