Acute respiratory distress syndrome (ARDS) is a common disease caused by direct lung injury or extra-pulmonary diseases and is often associated with high morbidity and mortality. Due to the diverse pathophysiology of ARDS among patients, challenges in identifying disease mechanisms and specific therapeutic interventions remain. In an effort to standardize preclinical observational conditions, a widely used animal model for ARDS/acute inflammation involves lipopolysaccharide (LPS) administration. Intravenous or intraperitoneal LPS administration can cause indirect lung and/or organ injury due to the release of inflammatory mediators into the systemic circulation.
Experimental animals: C57BL/6N, 6-weeks-old, female
Modeling reagent: Lipopolysaccharide (LPS, 13mg/kg) i.p.
Parameters measured: Body weight, survival rate
The acute inflammation mouse model was induced by intraperitoneal injection of lipopolysaccharide (LPS, 13mg/kg) on day 0. Dexamethasone (1.2mg/kg, i.p.) or an anti-TLR4 antibody (10mg/kg, i.p.) was injected the day before LPS induction. Survival rate and body weight were measured daily.
Efficacy Evaluation in LPS-Induced Acute Inflammatory Mice
Efficacy evaluation in an acute inflammation mouse model induced by LPS. (A) Body weight and percent of body weight change, (B) survival rate, (C) and mIL6 serum levels were measured in mice following LPS induction. Dexamethasone and anti-TLR4 Ab treatment improved survival rate and decreased serum mIL6 levels in LPS mice.