Lim Seung Hyuk, Jung Harry, Youn Dong Hyuk, Kim Tae Yeon, Han Sung Woo, Kim Bong Jun, Lee Jae Jun, Jeon Jin Pyeong
Institute of New Frontier Research, Hallym University College of Medicine, Chuncheon, Korea.
Department of Neurosurgery, Hallym University College of Medicine, Chuncheon, Korea.
J Korean Neurosurg Soc. 2022 Sep;65(5):680-687. doi: 10.3340/jkns.2021.0310. Epub 2022 May 16.
The influence of moderate-to-severe traumatic brain injury (TBI) on acute pulmonary injury is well established, but the association between acute pulmonary injury and mild TBI has not been well studied. Here, we evaluated the histological changes and fluctuations in inflammatory markers in the lungs to determine whether an acute pulmonary inflammatory response occurred after mild TBI.
Mouse models of mild TBI (n=24) were induced via open-head injuries using a stereotaxic impactor. The brain and lungs were examined 6, 24, and 72 hours after injury and compared to sham-operated controls (n=24). Fluoro-Jade B staining and Astra blue and hematoxylin staining were performed to assess cerebral neuronal degeneration and pulmonary histological architecture. Quantitative real-time polymerase chain reaction analysis was done to measure inflammatory cytokines.
Increased neuronal degeneration and the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β were observed after mild TBI. The IL-6, TNF-α, and TGF-β levels in mice with mild TBI were significantly different compared to those of sham-operated mice 24 hours after injury, and this was more pronounced at 72 hours. Mild TBI induced acute pulmonary interstitial edema with cell infiltration and alveolar morphological changes. In particular, a significant infiltration of mast cells was observed. Among the inflammatory cytokines, TNF-α was significantly increased in the lungs at 6 hours, but there was no significant difference 24 and 72 hours after injury.
Mild TBI induced acute pulmonary interstitial inflammation and alveolar structural changes, which are likely to worsen the patient's prognosis.
中重度创伤性脑损伤（TBI）对急性肺损伤的影响已得到充分证实，但急性肺损伤与轻度TBI之间的关联尚未得到充分研究。在此，我们评估了肺部的组织学变化和炎症标志物的波动情况，以确定轻度TBI后是否发生急性肺部炎症反应。
通过使用立体定位撞击器进行开放性颅脑损伤诱导建立轻度TBI小鼠模型（n = 24）。在损伤后6、24和72小时检查脑和肺，并与假手术对照组（n = 24）进行比较。进行氟玉髓B染色以及阿斯特拉蓝和苏木精染色以评估脑神经元变性和肺组织学结构。进行定量实时聚合酶链反应分析以测量炎症细胞因子。
轻度TBI后观察到神经元变性增加以及白细胞介素（IL）-6、肿瘤坏死因子（TNF）-α、IL-10和转化生长因子（TGF）-β的mRNA表达增加。轻度TBI小鼠在损伤后24小时时IL-6、TNF-α和TGF-β水平与假手术小鼠相比有显著差异，在72小时时更为明显。轻度TBI诱导急性肺间质水肿伴细胞浸润和肺泡形态改变。特别是，观察到肥大细胞有显著浸润。在炎症细胞因子中，TNF-α在损伤后6小时时在肺中显著增加，但在损伤后24和72小时时无显著差异。
轻度TBI诱导急性肺间质炎症和肺泡结构改变，这可能会使患者的预后恶化。
