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Updated: Jun 15, 2025

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Lactic acid regulates lipid droplet aggregation through a microglia-neuron axis in neuroinflammation
Zhuoqing Lan1, Shukai Lv2, Ziyi Ge3
1Department of Anesthesiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China; Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, China.
None:
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.
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