Endotoxin-induced microvascular lung injury in mice is a commonly used experimental model of the acute respiratory distress syndrome (ARDS). The present paper aimed to characterize this popular model in a comprehensive and systematic fashion. Male C57bl/6 mice (n = 5) were administered an LD55 dose of E. coli endotoxin (15 mg/kg, i.p.), and lungs were harvested at several time points and evaluated for injury as well as for expression of a variety of inflammatory mediators. Endotoxin induced many features characteristic of acute microvascular lung injury. These included early (1-2 h) expression of inflammatory mediators (IL-1α, IL-1β, IL-4, IL-6, IL-10, TNF-α, interferon-α, interferon-γ, and MCP-1) and leukocyte accumulation in lung tissue (lung myeloperoxidase activity 18.5 ± 7.8 U/g tissue, P <0.05), followed by pulmonary edema (lung water content index 17.4% ± 2.5%, P <0.05) and mortality. Histopathological evaluation of lung tissue was compatible with these findings. The characterization of this murine model of endotoxin-induced microvascular injury will facilitate its utilization in ARDS research.
|Original language||English (US)|
|Number of pages||4|
|State||Published - Apr 2002|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine