Department of Anesthesiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China; Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, China.
Department of General Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
J Lipid Res. 2024 Oct;65(10):100629. doi: 10.1016/j.jlr.2024.100629. Epub 2024 Aug 23.
Neuroinflammation, marked by the release of proinflammatory cytokines and resulting neuronal death, is a multifaceted process extending beyond traditional inflammatory pathways. Microglia, primary cells in the inflammatory response, rapidly activate during neuroinflammation and produce proinflammatory and cytotoxic factors that affect neuronal function. Recent evidence highlights the significant role of abnormal lipid droplet (LD) deposition in the pathogenesis of neuroinflammation. While microglia are known to influence LD aggregation during neuroinflammation, the regulatory mechanism within neurons is not well understood. Our study demonstrates that lipopolysaccharide-activated microglia induce the accumulation of LD in neurons, identifying microglial-derived lactic acid as a key mediator in this process. Excessive lipid accumulation threatens neuronal function, a phenomenon reversed by eliminating microglia. Our study demonstrates that lipopolysaccharide-activated microglia induce the accumulation of LD in neurons, identifying microglial-derived lactic acid as a key mediator in this process. Excessive lipid accumulation threatens neuronal function, a phenomenon reversed by eliminating microglia.
神经炎症是一个多方面的过程，其特征是释放促炎细胞因子并导致神经元死亡，它超越了传统的炎症途径。小胶质细胞是炎症反应中的主要细胞，在神经炎症中迅速激活，并产生促炎和细胞毒性因子，影响神经元功能。最近的证据强调了异常脂滴 (LD) 沉积在神经炎症发病机制中的重要作用。虽然已知小胶质细胞在神经炎症期间会影响 LD 的聚集，但神经元内的调节机制尚不清楚。我们的研究表明，脂多糖激活的小胶质细胞诱导神经元中 LD 的积累，确定小胶质细胞衍生的乳酸是这一过程中的关键介质。过多的脂质积累会威胁神经元功能，而消除小胶质细胞则可以逆转这一现象。
