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1 Department of Medicine, Keio University, School of Medicine, Tokyo, Tokyo, Japan
2 Department of Anesthesiology6, Kyoto Prefectural University of Medicine, Kyoto, Kyoto, Japan
3 Department of Pediatrics and Medicine, University of Utah, School of Medicine, Salt Lake City, UT, USA
4 Department of Molecular and Internal Medicine, Hiroshima University, Graduate School of Biomedical Science, Hiroshima, Hiroshima, Japan
5 Department of Anesthesiology, Keio University, School of Medicine, Tokyo, Tokyo, Japan
6 Department of Medicine and Anesthesia, University of California at San Francisco, Cardiovascular Research Institute, San Francisco, CA, USA
7 Department of Medicine, VA/Puget Sound Medical Center, Primary and Specialty Medicine Service Line, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: ishiz{at}attglobal.net.
KL-6 is a pulmonary epithelial mucin more prominently expressed on the surface membrane of alveolar type II cells when these cells are proliferating, stimulated and/or injured. We hypothesized that high levels of KL-6 in epithelial lining fluid and plasma would reflect the severity of lung injury in patients with acute lung injury (ALI). Epithelial lining fluid was obtained at onset (day 0) and day 1 of ARDS/ALI by bronchoscopic microsampling procedure in 35 patients. On day 0, KL-6 and albumin concentrations in epithelial lining fluid were significantly higher than in normal controls (P <0.001), and the concentrations of KL-6 in epithelial lining fluid (P <0.002) and in plasma (P <0.0001) were higher in non-survivors than in survivors of ALI/ARDS. These observations were corroborated by the immunohistochemical localization of KL-6 protein expression in the lungs of non-survivors with acute lung injury, and KL-6 secretion from cultured human alveolar type II cells stimulated by proinflammatory cytokines. Since injury to distal lung epithelial cells, including alveolar type II cells, is important in the pathogenesis of acute lung injury, the elevation of KL-6 concentrations in plasma and epithelial lining fluid could be valuable indicators for poor prognosis in clinical acute lung injury.
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