Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 75-83 |
| Number of pages | 9 |
| Journal | Respiratory Physiology and Neurobiology |
| Volume | 191 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2014 Jan 15 |
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Keywords
- Lung injury model
- Myeloperoxidase
- Neutrophil recruitment
- Oxidative stress marker
- Reactive oxygen species
ASJC Scopus subject areas
- Physiology
- Pulmonary and Respiratory Medicine
- Neuroscience(all)
- Medicine(all)
Cite this
Relationship between neutrophil influx and oxidative stress in alveolar space in lipopolysaccharide-induced lung injury. / Yoshida, T.; Nagai, K.; Inomata, T.; Ito, Y.; Betsuyaku, Tomoko; Nishimura, M.
In: Respiratory Physiology and Neurobiology, Vol. 191, No. 1, 15.01.2014, p. 75-83.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Relationship between neutrophil influx and oxidative stress in alveolar space in lipopolysaccharide-induced lung injury
AU - Yoshida, T.
AU - Nagai, K.
AU - Inomata, T.
AU - Ito, Y.
AU - Betsuyaku, Tomoko
AU - Nishimura, M.
PY - 2014/1/15
Y1 - 2014/1/15
N2 - 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.
AB - 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.
KW - Lung injury model
KW - Myeloperoxidase
KW - Neutrophil recruitment
KW - Oxidative stress marker
KW - Reactive oxygen species
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UR - http://www.scopus.com/inward/citedby.url?scp=84890331050&partnerID=8YFLogxK
U2 - 10.1016/j.resp.2013.11.008
DO - 10.1016/j.resp.2013.11.008
M3 - Article
VL - 191
SP - 75
EP - 83
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
SN - 1569-9048
IS - 1
ER -