吸入脂多糖诱导小鼠急性肺炎模型的建立

A mouse model of acute lung inflammation induced by lipopolysaccharide inhalation

目的:用吸入脂多糖(lipopolysaccharide,LPS)的方法建立简便、经济、稳定的小鼠急性肺炎模型。方法:将正常BALB/c小鼠麻醉后仰位固定,行LPS(50μL,1g/L)吸入,于不同时间点获取支气管肺泡灌洗液(bron-choalveolar lavage fluid,BALF)后取肺组织制备匀浆,对支气管肺泡灌洗液进行细胞染色分类计数,用ELISA的方法检测肺组织匀浆和支气管肺泡灌洗液白介素-1β((interleukin-1β,IL-1β)的含量。再取肺组织固定、切片,用HE染色鉴定炎症程度。结果:LPS吸入2～4h后,支气管肺泡灌洗液和肺组织匀浆中IL-1β水平即明显增加。2h时肺内就开始出现炎性细胞浸润,12～24h炎症加剧甚至形成脓肿。支气管肺泡灌洗液中中性粒细胞增多最早出现,从2h即开始增加,巨噬细胞和淋巴细胞则在1d后开始明显增加,一直持续3d。结论:用LPS吸入的方法可以建立快速、稳定、典型的小鼠急性肺炎模型。

Objective：To develop a convenient, economical and stable model of acute lung inflammation in mice. Methods： BALB/c mice were inhaled intranasally with 50 μL of LPS （1 g/L） or sterile PBS, and sacrificed at different time points after being anaesthetized. The bronchoalveolar lavage fluid （BALF） was collected, and the lungs were separated and homogenated or embedded and sliced to 5 μm sections, which were then stained by HE to determine the severity of inflammation. The inflammatory cell infiltration in bronehoalveolar lavage was counted and IL-1 β, the pro-inflammatory cytokine, measured by ELISA in lung homogenate and BALF. Results： The data showed that administration with 50 μg of LPS （ 1 g/L） for 2 h resulted in significant inflammation in the lung. LPS mainly stimulated the recruitment of neutrophils within 24 h. And LPS was a quick revulsant of IL-1 β production in BALF and in lung tissue between 4 and 24 h. Macrophages and lymphocytes recruited after 1 day, and sustained for at least 3 days. Conclusion： The results indicate that intranasal administration of LPS can induce a rapid and stable acute inflammatory model in mice.