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- Richard D Sue
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- John A Belperio
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Marie D Burdick
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Lynne A Murray
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Ying Ying Xue
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Maria C Dy
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Jeffery J Kwon
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Michael P Keane
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
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- Robert M Strieter
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California , Los Angeles, CA 90095
書誌事項
- 公開日
- 2004-03
- 権利情報
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- https://academic.oup.com/pages/standard-publication-reuse-rights
- DOI
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- 10.4049/jimmunol.172.6.3860
- 公開者
- Oxford University Press (OUP)
この論文をさがす
説明
<jats:title>Abstract</jats:title> <jats:p>Hyperoxia-induced lung injury is characterized by infiltration of activated neutrophils in conjunction with endothelial and epithelial cell injury, followed by fibrogenesis. Specific mechanisms recruiting neutrophils to the lung during hyperoxia-induced lung injury have not been fully elucidated. Because CXCL1 and CXCL2/3, acting through CXCR2, are potent neutrophil chemoattractants, we investigated their role in mediating hyperoxia-induced lung injury. Under variable concentrations of oxygen, murine survival during hyperoxia-induced lung injury was dose dependent. Eighty percent oxygen was associated with 50% mortality at 6 days, while greater oxygen concentrations were more lethal. Using 80% oxygen, we found that lungs harvested at day 6 demonstrated markedly increased neutrophil sequestration and lung injury. Expression of CXCR2 ligands paralleled neutrophil recruitment to the lung and CXCR2 mRNA expression. Inhibition of CXC chemokine ligands/CXCR2 interaction using CXCR2−/− mice exposed to hyperoxia significantly reduced neutrophil sequestration and lung injury, and led to a significant survival advantage as compared with CXCR2+/+ mice. These findings demonstrate that CXC chemokine ligand/CXCR2 biological axis is critical during the pathogenesis of hyperoxia-induced lung injury.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 172 (6), 3860-3868, 2004-03
Oxford University Press (OUP)