Relationship between neutrophil influx and oxidative stress in alveolar space in lipopolysaccharide-induced lung injury

- There was a timing difference between lung injury and alveolar neutrophil infiltration.
- Lung injury increased even after neutrophils disappearance in BAL fluid.
- BAL neutrophils generated more MPO activity and ROS at later time point.
- Alveolar oxidative stress and MPO activity persisted longer in ARDS.

We intratracheally administered lipopolysaccharide (LPS) to ICR mice and then collected BAL fluid and lung tissue to determine whether levels of neutrophils and/or myeloperoxidase (MPO) in bronchoalveolar lavage (BAL) fluid reflect lung tissue damage. Robust neutrophil accumulation into the alveolar space and lung tissue were almost completely abolished at seven days along with oxidative stress markers in the lung. However, lung injury scores and lung wet/dry ratios, as well as MPO and oxidative stress markers in BAL fluid were significantly increased at five and seven days after LPS administration. At later time points, BAL neutrophils generated more MPO activity and ROS than those harvested sooner after LPS administration. Although elevated neutrophil levels in BAL fluid reflected oxidative stress in the lungs, MPO might serve as a useful marker to evaluate damage sustained by epithelial cells over the long term.