[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.


CONCLUSIONS
The results indicate that intranasal administration of LPS can induce a rapid and stable acute inflammatory model in mice.
Department of Physiology and Pathophysiology, Peking University School of Basic Medical Science, Beijing 100191, China.
Ling
L
Guo
Wen-jing
WJ
Li
Ming-jiang
MJ
Xu
Xian
X
Wang
D000208:Acute Disease; D000280:Administration, Inhalation; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004195:Disease Models, Animal; D005260:Female; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011014:Pneumonia / Q000139:chemically induced*; D011897:Random Allocation
D008070:Lipopolysaccharides