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The role of inflammation in secondary pathology following central nervous system injury.

机译：中枢神经系统损伤后炎症在继发性病理中的作用。

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摘要

Injury to the adult mammalian central nervous system leads to a complex series of cellular and molecular reactions as damaged tissue attempts to repair, reorganize, and restore normal physiological functions. For over a century, scientists have conducted experiments investigating the wound healing responses of the brain and spinal cord in an effort to understand why the central nervous system does not repair itself efficiently after traumatic injury. The experiments presented in this thesis demonstrate that inflammation plays a key role in the secondary pathological changes which are seen in the central nervous system following trauma. The results illustrate the upregulation of extracellular matrix molecules in the presence of post-traumatic inflammatory infiltrates, and document the association of inhibitory proteoglycans with the borders of enlarging cavities in the brain and spinal cord. Utilizing minimally invasive techniques to avoid primary physical injury, this study demonstrates in vivo that inflammatory processes alone initiate a cascade of secondary tissue damage, progressive cavitation, and glial scarring in the central nervous system. An in vitro model is described which shows that macrophage inflammatory activation initiates secondary neuropathology. A novel mechanism of inflammation-induced cavitation is described using time-lapse video analysis which shows astrocyte morphological changes and migration that lead to astrocyte abandonment of neuronal processes, neurite stretching, and secondary injury. The macrophage mannose receptor and the CR3 beta2-integrin are implicated in the cascade which induces cavity and scar formation. Finally, a potential new anti-inflammatory therapeutic treatment has been proposed to minimize post-traumatic inflammatory damage utilizing agonists to the PPAR-gamma nuclear hormone receptor. These studies demonstrate the destructive effects of persistent inflammation in the development of secondary pathology within the central nervous system, and provide encouraging results that suggest that modulation of the acute inflammatory response may be an important therapeutic target for preventing detrimental responses to injury in the central nervous system.
机译：当受损的组织试图修复，重组和恢复正常的生理功能时，成年哺乳动物中枢神经系统的损伤会导致一系列复杂的细胞和分子反应。一个多世纪以来，科学家们进行了一些实验，研究大脑和脊髓的伤口愈合反应，以了解为什么中枢神经系统在创伤后不能有效地自我修复。本文提出的实验表明，炎症在继发于中枢神经系统的继发性病理变化中起关键作用。结果说明在创伤后炎症浸润的存在下细胞外基质分子的上调，并证明抑制性蛋白聚糖与脑和脊髓腔增大的边界之间的关系。利用微创技术避免原发性身体伤害，这项研究在体内证明了炎症过程本身会引发继发性组织损伤，进行性空化和中枢神经系统神经胶质瘢痕形成。描述了一种体外模型，该模型显示巨噬细胞炎症激活引发继发性神经病理学。使用延时视频分析描述了炎症诱导的空化的新机制，该分析显示了星形胶质细胞形态变化和迁移，导致星形胶质细胞放弃了神经元过程，神经突伸展和继发性损伤。巨噬细胞甘露糖受体和CR3 beta2-整联蛋白牵涉级联反应，其诱导空腔和疤痕形成。最后，已经提出了潜在的新型抗炎治疗方法，以利用对PPAR-γ核激素受体的激动剂使创伤后的炎性损害最小化。这些研究表明持续炎症对中枢神经系统继发性病理的破坏作用，并提供令人鼓舞的结果，表明急性炎症反应的调节可能是预防中枢神经损伤的有害反应的重要治疗靶点。系统。

著录项

  • 作者

    Fitch, Michael Thomas.;

  • 作者单位

    Case Western Reserve University (Health Sciences).;

  • 授予单位 Case Western Reserve University (Health Sciences).;
  • 学科 Biology Neuroscience.
  • 学位 Ph.D.
  • 年度 1999
  • 页码 179 p.
  • 总页数 179
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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