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

被引:20
|
作者
Yoshida, T. [1 ]
Nagai, K. [1 ]
Inomata, T. [1 ]
Ito, Y. [1 ]
Betsuyaku, T. [2 ]
Nishimura, M. [1 ]
机构
[1] Hokkaido Univ, Sch Med, Dept Med 1, Sapporo, Hokkaido 0608638, Japan
[2] Keio Univ, Sch Med, Dept Med, Div Pulm Med, Tokyo 160, Japan
基金
日本学术振兴会;
关键词
Oxidative stress marker; Neutrophil recruitment; Myeloperoxidase; Reactive oxygen species; Lung injury model; RESPIRATORY-DISTRESS-SYNDROME; BRONCHOALVEOLAR LAVAGE FLUID; CD11B/CD18; INTEGRINS; SERUM-ALBUMIN; MYELOPEROXIDASE; INFLAMMATION; MACROPHAGES; GLUTATHIONE; CARBONYLATION; PERMEABILITY;
D O I
10.1016/j.resp.2013.11.008
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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. (C) 2013 Elsevier B.V. All rights reserved.
引用
收藏
页码:75 / 83
页数:9
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