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Published ahead of print on February 2, 2006, doi:10.1164/rccm.200509-1477OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 9, May 2006, 1008-1015

A more recent version of this article appeared on May 1, 2006
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Submitted on September 21, 2005
Accepted on February 2, 2006

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

Tokujiro Uchida1*, Madoka Shirasawa1, Lorraine B Ware2, Katsuo Kojima3, Yutaka Hata4, Koshi Makita1, Gabe Mednick5, Zachary A Matthay5, and Michael A Matthay5

1 Department of Anesthesiology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan, 2 Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA, 3 Department of Cardiothoracic Surgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan, 4 Department of Medical Biochemistry, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan, 5 Departments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA

* To whom correspondence should be addressed. 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 either 10 mg/kg lipopolysaccharide (LPS) 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 (IQR; 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 as well as in patients with acute lung injury.
Key words: acute respiratory distress syndrome, biological markers, alveolar epithelium, pulmonary edema




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