Intraperitoneal instillation versus intratracheal injection of lipopolysaccharide: differences in establishment of acute lung injury model_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

YUAN Weifeng ¹ , LI Li ¹ , XU Hong ¹ , HU Yujie ² ,  HUANG Wenjie ¹

1. Department of Respiratory Medicine, Guangzhou General Hospital of Guangzhou Military command, Guangzhou, Guangdong 510010, P.R.China;
2. Department of Respiratory Medicine, 458^th Hospital of PLA, Guangzhou, Guangdong 510062, P.R.China;

Corresponding author：

HUANG Wenjie, Email: huangyelu1029@vip.163.com

Keywords：

Acute lung injury; Animal model; Intratracheal instillation; Intraperitoneal injection; Lipopolysaccharide

DOI：

10.7507/1671-6205.201610045

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ObjectiveTo compare two different ways to establish mouse model with acute lung injury (ALI) via intratracheal instillation or intraperitoneal injection of lipopolysaccharide (LPS). MethodsBALB/c mice received intraperitoneal/intratracheal administration of LPS or sham operation. Wet/dry lung weight ratio, protein concentration in bronchoalveolar lavage fluid (BALF), and lung tissue histology were examined at 0, 1, 2, 6, 12, 18, 24, 48 h after LPS administration. Tumor necrosis factor-α (TNF-α) in BALF and serum was assayed with ELISA method. ResultsLPS treatment significantly increased wet/dry lung weight ratio, BALF protein concentration and TNF-α concentration in serum and BALF. Lung tissue was damaged after LPS challenge. The mice received LPS intraperitoneal injection got a more significant lung edema than those received LPS intratracheal instillation. Inversely, LPS intratracheal instillation induced more severed microstructure destruction. ConclusionsALI animal model by LPS intratracheal instillation or intraperitoneal injection induces inflammation and tissue damage in lung. However, the degree of tissue damage or self-healing induced by two methods is different. Therefore the decision of which way to establish ALI model will depend on the study purpose.

Citation： YUAN Weifeng, LI Li, XU Hong, HU Yujie, HUANG Wenjie. Intraperitoneal instillation versus intratracheal injection of lipopolysaccharide: differences in establishment of acute lung injury model. Chinese Journal of Respiratory and Critical Care Medicine, 2017, 16(3): 274-279. doi: 10.7507/1671-6205.201610045 Copy

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9.	梁颖红, 龚艳杰, 刘佳, 等. 输血相关急性肺损伤大鼠肺组织细胞因子诱导的中性粒细胞趋化因子的表达. 中国呼吸与危重监护杂志, 2016, 15(4): 379-383.
10.	Chu SJ, Perng WC, Hung CM, et al. Effects of various body temperatures after lipopolysaccharide-induced lung injury in rats. Chest, 2005, 128(1): 327-336.
11.	盖菁菁, 王金平, 王娟, 等. 急性肺损伤大鼠肺组织中颗粒溶素的表达. 中国呼吸与危重监护杂志, 2012, 11(3): 282-285.

1. Schuster DP. What is acute lung injury?. Chest, 1995, 107(6): 1721-1726.
2. 李洪霞, 张进川, 刘岩. 气管滴入及腹腔注入内毒素致大鼠急性肺损伤机制的研究. 军医进修学院学报, 2003, 24(1): 4-6.
3. Mikawa K, Nishina K, Takao Y, et al. ONO-1714, a nitric oxide synthase inhibitor, attenuates endotoxin-induced acute lung injury in rabbits. Anesth Analg, 2003, 97(6): 1751-1755.
4. 马李杰, 李王平. 金发光急性肺损伤/急性呼吸窘迫综合征发病机制的研究进展. 中华肺部疾病杂志(电子版), 2013, 6(1): 65-68.
5. 陈娇, 钱晓明, 聂时南. 急性肺损伤动物模型的研究现状. 医学研究生学报, 2013, 26(8): 851-854.
6. 洪渊智, 李娜萍, 吴人亮, 等. β-连环素及相关蛋白在脂多糖致急性肺损伤小鼠气道上皮的表达. 华中科技大学学报(医学版), 2007, 36(4): 421-424.
7. Mei SHJ, McCarter SD, Deng Y, et al. Prevention of LPS-induced acute lung injury in mice by mesenchymal stem cells overexpressing angiopoietin 1. PLoS Med, 2007, 4(9): 1525-1537.
8. 朱桂军, 于占彪, 胡振杰. 二烯丙基三硫对脂多糖诱导急性肺损伤小鼠肺组织 TNF-α 和 IL-1β 的影响. 河北医科大学学报, 2007, 28(4): 248-251.
9. 梁颖红, 龚艳杰, 刘佳, 等. 输血相关急性肺损伤大鼠肺组织细胞因子诱导的中性粒细胞趋化因子的表达. 中国呼吸与危重监护杂志, 2016, 15(4): 379-383.
10. Chu SJ, Perng WC, Hung CM, et al. Effects of various body temperatures after lipopolysaccharide-induced lung injury in rats. Chest, 2005, 128(1): 327-336.
11. 盖菁菁, 王金平, 王娟, 等. 急性肺损伤大鼠肺组织中颗粒溶素的表达. 中国呼吸与危重监护杂志, 2012, 11(3): 282-285.

Chinese Journal of Respiratory and Critical Care Medicine

Intraperitoneal instillation versus intratracheal injection of lipopolysaccharide: differences in establishment of acute lung injury model

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