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Published ahead of print on February 2, 2006, doi:10.1164/rccm.200509-1477OC
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American Journal of Respiratory and Critical Care Medicine Vol 173. pp. 1008-1015, (2006)
© 2006 American Thoracic Society
doi: 10.1164/rccm.200509-1477OC

Original Article

Receptor for Advanced Glycation End-Products Is a Marker of Type I Cell Injury in Acute Lung Injury

Tokujiro Uchida*, Madoka Shirasawa*, Lorraine B. Ware, Katsuo Kojima, Yutaka Hata, Koshi Makita, Gabe Mednick, Zachary A. Matthay and Michael A. Matthay

Departments of Anesthesiology, Cardiothoracic Surgery, and Medical Biochemistry, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; and Departments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California–San Francisco, San Francisco, California

Correspondence and requests for reprints should be addressed to Tokujiro Uchida, M.D., Department of Anesthesiology, Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. E-mail: uchida.mane{at}tmd.ac.jp

Rationale: Receptor for advanced glycation end-products (RAGE) is one of the alveolar type I cell–associated proteins in the lung.

Objectives: To test the hypothesis that RAGE is a marker of alveolar epithelial type I cell injury.

Methods: Rats were instilled intratracheally with 10 mg/kg lipopolysaccharide or hydrochloric acid. RAGE levels were measured in the bronchoalveolar lavage (BAL) and serum in the rats and in the pulmonary edema fluid and plasma from patients with acute lung injury (ALI; n = 22) and hydrostatic pulmonary edema (n = 11).

Main Results: In the rat lung injury studies, RAGE was released into the BAL and serum as a single soluble isoform sized ~ 48 kD. The elevated levels of RAGE in the BAL correlated well with the severity of experimentally induced lung injury. In the human studies, the RAGE level in the pulmonary edema fluid was significantly higher than the plasma level (p < 0.0001). The median edema fluid/plasma ratio of RAGE levels was 105 (interquartile range, 55–243). The RAGE levels in the pulmonary edema fluid from patients with ALI were higher than the levels from patients with hydrostatic pulmonary edema (p < 0.05), and the plasma RAGE level in patients with ALI were significantly higher than the healthy volunteers (p < 0.001) or patients with hydrostatic pulmonary edema (p < 0.05).

Conclusion: RAGE is a marker of type I alveolar epithelial cell injury based on experimental studies in rats and in patients with ALI.

Key Words: acute respiratory distress syndrome • alveolar epithelium • biological markers • pulmonary edema




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