Department of Human Anatomy, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Anat Rec (Hoboken). 2012 Sep;295(9):1513-9. doi: 10.1002/ar.22531. Epub 2012 Jul 12.
Animal model is of importance to further elucidate the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). We envisioned a possibility that there might be the differences in lipopolysaccharide (LPS)-induced acute lung inflammation by the trans-oral and trans-tracheal intratracheal instillations. We compared the LPS-induced early inflammatory responses by these two methods. The evaluative system included bronchoalveolar lavage (BAL) fluid biochemical analysis and differential cell counting, lung wet/dry weight ratio and lung histology. In vitro studies were performed on human bronchial epithelial cell line NCI-H292 and alveolar Type II epithelial cell line A549 stimulated with LPS. Both interleukin (IL)-8 release in the BAL fluid and IL-8 secretions from NCI-H292 and A549 cells were measured. We found that the trans-tracheal intratracheal instillation promoted the LPS-induced cell injury, neutrophil infiltration, and pulmonary edema compared to the trans-oral one. The LPS-induced pathological changes by the trans-oral intratracheal instillation were characterized by pulmonary interstitial edema, but the trans-tracheal intratracheal instillation was exudative pulmonary edema. More IL-8 is produced from A549 cells than from NCI-H292 cells under the treatment of LPS. The increased IL-8 release in the BAL fluid and enhanced inflammatory responses caused by LPS may be due to more LPS delivered into the alveolar spaces by the trans-tracheal intratracheal instillation compared to the trans-oral one. The trans-tracheal intratracheal instillation is proved to be more suitable to establish the murine model of ALI than the trans-oral one and helpful to further elucidate the pathogenesis of ALI/ARDS.
动物模型对于进一步阐明急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDS）的发病机制具有重要意义。我们设想，经口和经气管两种气管内滴注方式可能会导致脂多糖（LPS）诱导的急性肺炎症存在差异。我们比较了这两种方法诱导的 LPS 早期炎症反应。评估系统包括支气管肺泡灌洗液（BAL）生化分析和细胞分类计数、肺湿/干重比和肺组织学。体外研究采用 LPS 刺激的人支气管上皮细胞系 NCI-H292 和肺泡Ⅱ型上皮细胞系 A549 进行。测量 BAL 液中白细胞介素（IL）-8 释放和 NCI-H292 和 A549 细胞的 IL-8 分泌。我们发现，与经口气管内滴注相比，经气管气管内滴注促进了 LPS 诱导的细胞损伤、中性粒细胞浸润和肺水肿。经口气管内滴注诱导的 LPS 病理变化表现为肺间质水肿，而经气管气管内滴注则为渗出性肺水肿。在 LPS 处理下，A549 细胞产生的 IL-8 多于 NCI-H292 细胞。BAL 液中 IL-8 释放增加和 LPS 引起的炎症反应增强可能是由于经气管气管内滴注比经口气管内滴注将更多 LPS 递送至肺泡空间所致。与经口气管内滴注相比，经气管气管内滴注更适合建立 ALI 小鼠模型，有助于进一步阐明 ALI/ARDS 的发病机制。
