title: Relationship between neutrophil influx and oxidative stress in alveolar space in lipopolysaccharide-induced lung injury.
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.
authors.affiliation: First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshida
authors.affiliation: First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan. Electronic address: katnagai@med.hokudai.ac.jp.
authors.forename: K
authors.initials: K
authors.lastname: Nagai
authors.affiliation: First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Inomata
authors.affiliation: First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ito
authors.affiliation: Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Betsuyaku
authors.affiliation: First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nishimura
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005434:Flow Cytometry; D016179:Granulocyte Colony-Stimulating Factor / Q000378:metabolism; D007377:Interleukin-3 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D055370:Lung Injury / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology*; D050050:Protein Carbonylation / Q000187:drug effects; D011650:Pulmonary Alveoli / Q000473:pathology*; D011654:Pulmonary Edema / Q000209:etiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D013053:Spectrophotometry; D013997:Time Factors
chemical_list: D000447:Aldehydes; C503133:Gr-1 protein, mouse; D007377:Interleukin-3; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D019707:Receptors, Chemokine; D011993:Recombinant Fusion Proteins; C404145:myelopoietin; D016179:Granulocyte Colony-Stimulating Factor; C027576:4-hydroxy-2-nonenal
keywords: Lung injury model; Myeloperoxidase; Neutrophil recruitment; Oxidative stress marker; Reactive oxygen species