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<p>To study dynamic changes in microglia/monocyte cell populations and to assess the state of neurons, a model of traumatic brain injury (TBI) in C57BL/6 mice was used. TBI was induced by modeling controlled cortical damage. Microglia/monocyte distribution was assessed using a combination of histological and immunohistochemical methods, including analysis of the expression of specific cellular markers. In the acute phase of TBI, a significant increase in the expression of MHC II (a marker of the major histocompatibility complex class II) and the cell surface marker CD68 was observed, indicating the activation of proinflammatory microglia/monocytes, as well as an increase in the level of Iba-1 (a marker of the total pool of microglia/monocytes) in the area of injury. Over the next 56 days after injury, a gradual decrease in the expression of these markers was observed, which was accompanied by characteristic histological changes. In addition, changes in the expression of NeuN (a neuronal marker) and ATF3 (a marker of neuronal stress and regeneration) were detected, indicating the state of neurons. Taken together, these results demonstrate that dynamic changes in microglial/monocyte and neuronal populations mediate the pathophysiological processes underlying the clinical manifestations of TBI.</p>

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Temporal Dynamics of Neuroinflammation after Cortical Injury in Mice

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • I. V. Manzhulo,
  • A. A. Tyrtyshnaia,
  • F. K. Avgustinovich,
  • O. S. Manzhulo,
  • E. S. Gromova,
  • D. N. Ivashkevich

摘要

To study dynamic changes in microglia/monocyte cell populations and to assess the state of neurons, a model of traumatic brain injury (TBI) in C57BL/6 mice was used. TBI was induced by modeling controlled cortical damage. Microglia/monocyte distribution was assessed using a combination of histological and immunohistochemical methods, including analysis of the expression of specific cellular markers. In the acute phase of TBI, a significant increase in the expression of MHC II (a marker of the major histocompatibility complex class II) and the cell surface marker CD68 was observed, indicating the activation of proinflammatory microglia/monocytes, as well as an increase in the level of Iba-1 (a marker of the total pool of microglia/monocytes) in the area of injury. Over the next 56 days after injury, a gradual decrease in the expression of these markers was observed, which was accompanied by characteristic histological changes. In addition, changes in the expression of NeuN (a neuronal marker) and ATF3 (a marker of neuronal stress and regeneration) were detected, indicating the state of neurons. Taken together, these results demonstrate that dynamic changes in microglial/monocyte and neuronal populations mediate the pathophysiological processes underlying the clinical manifestations of TBI.