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<p>Inflammation within the central nervous system (CNS) plays a pivotal role in neuronal survival and degeneration. Lipopolysaccharide (LPS) is a widely used agent for inducing systemic and localized inflammation in mammals, providing a model for studying neurodegenerative processes. While previous research has documented neuronal loss due to LPS-induced neurodegeneration, the progressive morphological changes in neurons remain insufficiently characterized, particularly in retinal tissues. This study addresses this gap by establishing acute and chronic retinal inflammation models in mice using single and repeated intraperitoneal LPS injections. Through ultrastructural analyses using electron microscopy, we observed significant pathological changes in retinal neurons, glial cells, and blood-retinal barrier (BRB) components. Acute LPS exposure resulted in lipid droplet accumulation and membrane disruption in retinal pigment epithelium (RPE), as well as abnormal neuronal and vascular ultrastructures. Chronic LPS exposure amplified these effects, causing more pronounced damage to neurons and exacerbating BRB dysfunction. This study provides, for the first time, detailed ultrastructural insights into LPS-induced acute and chronic retinal inflammation. These findings advance our understanding of retinal pathology in inflammatory conditions and support the development of novel therapeutic strategies for retinal and CNS neurodegenerative diseases.</p>

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Ultrastructural response of the retinal cells and neurovascular unit to neuroinflammation induced by lipopolysaccharide

  • 期刊论文

  • 发表日期：

    2026年6月14日

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  • Bilin Rao,
  • Xiaotian Wu,
  • Xiaoqing Liu,
  • Fenglan Wang,
  • Fang He,
  • Xin Lin,
  • Guiyu Guan,
  • Xiaoqian Lai,
  • Jun Zhang

摘要

Inflammation within the central nervous system (CNS) plays a pivotal role in neuronal survival and degeneration. Lipopolysaccharide (LPS) is a widely used agent for inducing systemic and localized inflammation in mammals, providing a model for studying neurodegenerative processes. While previous research has documented neuronal loss due to LPS-induced neurodegeneration, the progressive morphological changes in neurons remain insufficiently characterized, particularly in retinal tissues. This study addresses this gap by establishing acute and chronic retinal inflammation models in mice using single and repeated intraperitoneal LPS injections. Through ultrastructural analyses using electron microscopy, we observed significant pathological changes in retinal neurons, glial cells, and blood-retinal barrier (BRB) components. Acute LPS exposure resulted in lipid droplet accumulation and membrane disruption in retinal pigment epithelium (RPE), as well as abnormal neuronal and vascular ultrastructures. Chronic LPS exposure amplified these effects, causing more pronounced damage to neurons and exacerbating BRB dysfunction. This study provides, for the first time, detailed ultrastructural insights into LPS-induced acute and chronic retinal inflammation. These findings advance our understanding of retinal pathology in inflammatory conditions and support the development of novel therapeutic strategies for retinal and CNS neurodegenerative diseases.