• Ling Liu, Zhenping Gao, Changli Xia, Yanyan Xu, Zhongsen Ma, Chunling Dong, and Bo Li.
• Department of Human Anatomy, Norman Bethune College of Medicine, Jilin University, Changchun, China.
• Anat Rec (Hoboken). 2012 Sep 1;295(9):1513-9.

AbstractAnimal 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.Copyright © 2012 Wiley Periodicals, Inc.

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