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

Video：

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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.	梁穎紅, 龔艷杰, 劉佳, 等. 輸血相關急性肺損傷大鼠肺組織細胞因子誘導的中性粒細胞趨化因子的表達. 中國呼吸與危重監護雜志, 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.	蓋菁菁, 王金平, 王娟, 等. 急性肺損傷大鼠肺組織中顆粒溶素的表達. 中國呼吸與危重監護雜志, 2012, 11(3): 282-285.

1. Schuster DP. What is acute lung injury?. Chest, 1995, 107(6): 1721-1726.
2. 李洪霞, 張進川, 劉巖. 氣管滴入及腹腔注入內毒素致大鼠急性肺損傷機制的研究. 軍醫進修學院學報, 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. 馬李杰, 李王平. 金發光急性肺損傷/急性呼吸窘迫綜合征發病機制的研究進展. 中華肺部疾病雜志(電子版), 2013, 6(1): 65-68.
5. 陳嬌, 錢曉明, 聶時南. 急性肺損傷動物模型的研究現狀. 醫學研究生學報, 2013, 26(8): 851-854.
6. 洪淵智, 李娜萍, 吳人亮, 等. β-連環素及相關蛋白在脂多糖致急性肺損傷小鼠氣道上皮的表達. 華中科技大學學報(醫學版), 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. 朱桂軍, 于占彪, 胡振杰. 二烯丙基三硫對脂多糖誘導急性肺損傷小鼠肺組織 TNF-α 和 IL-1β 的影響. 河北醫科大學學報, 2007, 28(4): 248-251.
9. 梁穎紅, 龔艷杰, 劉佳, 等. 輸血相關急性肺損傷大鼠肺組織細胞因子誘導的中性粒細胞趨化因子的表達. 中國呼吸與危重監護雜志, 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. 蓋菁菁, 王金平, 王娟, 等. 急性肺損傷大鼠肺組織中顆粒溶素的表達. 中國呼吸與危重監護雜志, 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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