Joo Jin, Jeong Jongmin, Park Hue Jung
Department of Anesthesiology and Pain Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Diagnostics (Basel). 2023 Feb 12;13(4):693. doi: 10.3390/diagnostics13040693.
Parkinson's disease (PD) is the second most common inflammatory neurodegenerative disorder after dementia. Preclinical and epidemiological data strongly suggest that chronic neuroinflammation slowly induces neuronal dysfunction. Activated microglia secrete several neurotoxic substances, such as chemokines and proinflammatory cytokines, which may promote blood-brain barrier (BBB) permeabilization. CD4 T cells comprise proinflammatory cells such as T helper (Th) 1 and Th17 cells, as well as anti-inflammatory cells such as Th2 and T regulatory cells (Tregs). Th1 and Th17 cells can be detrimental to dopamine neurons, whereas Th2 and Tregs are neuroprotective. The results of studies on the serum levels of cytokines such as IFN-γ and TNF-α secreted by Th1 T cells, IL-8 and IL-10 secreted by Th2 T cells, and IL-17 secreted by Th17 cells in PD patients are not uniform. In addition, the relationships between serum cytokine levels and motor and non-motor symptoms of PD are controversial. Surgical stress and anesthesia induce inflammatory responses by disturbing the balance between pro- and anti-inflammatory cytokines, which may exacerbate the neuroinflammatory response in PD patients. Here we review studies on blood inflammatory biomarkers in PD patients and discuss the roles of surgery and anesthesia in PD progression.
帕金森病（PD）是仅次于痴呆症的第二常见的炎症性神经退行性疾病。临床前和流行病学数据有力地表明，慢性神经炎症会缓慢诱导神经元功能障碍。活化的小胶质细胞会分泌几种神经毒性物质，如趋化因子和促炎细胞因子，这些物质可能会促进血脑屏障（BBB）通透性增加。CD4 T细胞包括促炎细胞，如辅助性T（Th）1细胞和Th17细胞，以及抗炎细胞，如Th2细胞和调节性T细胞（Tregs）。Th1和Th17细胞可能对多巴胺神经元有害，而Th2和Tregs具有神经保护作用。关于PD患者中Th1 T细胞分泌的细胞因子如IFN-γ和TNF-α、Th2 T细胞分泌的IL-8和IL-10以及Th17细胞分泌的IL-17的血清水平的研究结果并不一致。此外，血清细胞因子水平与PD的运动和非运动症状之间的关系也存在争议。手术应激和麻醉通过扰乱促炎和抗炎细胞因子之间的平衡诱导炎症反应，这可能会加剧PD患者的神经炎症反应。在此，我们综述了关于PD患者血液炎症生物标志物的研究，并讨论了手术和麻醉在PD进展中的作用。
