Cytokines, particularly IL-6, play a crucial role in modulating immune responses in the central nervous system (CNS). Elevated IL-6 levels have been observed in neuroinflammatory conditions, as well as in the sera and brains of patients with neurodegenerative diseases such as Parkinson's, Huntington's, Multiple Sclerosis, and Alzheimer's. Additionally, alterations in regional brain pH have been noted in these conditions. Acid-sensing ion channels (ASICs), including ASIC1a, activated by low pH levels, are highly abundant in the CNS and have recently been associated with various neurological disorders. Our study examined the impact of IL-6 on ASIC1a channels in cell cultures, demonstrating IL-6-induced the redistribution of cytosolic ASIC1a channels to the cell membrane. This redistribution was accompanied by increased ASIC1a current amplitude upon activation, as well as elevated levels of phosphorylated CaMKII and ERK kinases. Additionally, we observed posttranslational modifications on the ASIC1a channel itself. These findings provide insight into a potential link between inflammatory processes and neurodegenerative mechanisms, highlighting ASIC1a channels as promising therapeutic targets in these conditions.

细胞因子，特别是 IL-6，在调节中枢神经系统 (CNS) 的免疫反应中发挥着至关重要的作用。在神经炎症性疾病以及帕金森氏症、亨廷顿氏症、多发性硬化症和阿尔茨海默氏症等神经退行性疾病患者的血清和大脑中观察到 IL-6 水平升高。此外，在这些情况下，大脑区域 pH 值发生了变化。酸敏感离子通道 (ASIC)，包括由低 pH 水平激活的 ASIC1a，在中枢神经系统中含量丰富，最近与各种神经系统疾病相关。我们的研究检查了细胞培养物中 IL-6 对 ASIC1a 通道的影响，证明 IL-6 诱导胞质 ASIC1a 通道重新分布到细胞膜。这种重新分布伴随着激活后 ASIC1a 电流幅度的增加，以及磷酸化 CaMKII 和 ERK 激酶水平的升高。此外，我们还观察到 ASIC1a 通道本身的翻译后修改。这些发现提供了对炎症过程和神经退行性机制之间潜在联系的深入了解，强调 ASIC1a 通道是这些疾病中有希望的治疗靶点。