[A mouse model of acute lung inflammation induced by lipopolysaccharide inhalation].

OBJECTIVE: To develop a convenient, economical and stable model of acute lung inflammation in mice. METHODS: BALB/c mice were inhaled intranasally with 50 microL 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 mum sections, which were then stained by HE to determine the severity of inflammation. The inflammatory cell infiltration in bronchoalveolar lavage was counted and IL-1beta, the pro-inflammatory cytokine, measured by ELISA in lung homogenate and BALF. RESULTS: The data showed that administration with 50 microg 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-1beta 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.