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Published ahead of print on June 5, 2008, doi:10.1164/rccm.200707-1069OC

Am. J. Respir. Crit. Care Med., Volume 178, Number 4, August 2008, 356-362

A more recent version of this article appeared on August 15, 2008
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Submitted on July 20, 2007
Accepted on May 30, 2008

Role of Soluble Receptor for Advanced Glycation End-Products on Endotoxin-Induced Lung Injury

Haiying Zhang1, Sadatomo Tasaka2*, Yoshiki Shiraishi2, Koichi Fukunaga2, Wakako Yamada2, Hiroyuki Seki3, Yuko Ogawa2, Keisuke Miyamoto2, Yasushi Nakano2, Naoki Hasegawa2, Taku Miyasho4, Ikuro Maruyama5, and Akitoshi Ishizaka2

1 Division of Pulmonary Medicine, Keio University School of Medicine, Tokyo, Japan; Emergency Department, The First Affiliated Hospital, China Medical University, Shenyang, China, 2 Division of Pulmonary Medicine, Keio University School of Medicine, Tokyo, Japan, 3 Department of Anesthesiology, Keio University School of Medicine, Tokyo, Japan, 4 Laboratory of Veterinary Biochemistry, Rakuno Gakuen University, Ebetsu, Japan, 5 Department of Laboratory and Molecular Medicine, Kagoshima University, Kagoshima, Japan

* To whom correspondence should be addressed. E-mail: tasaka{at}cpnet.med.keio.ac.jp.

Rationale: The interaction of receptor for advanced glycation end-products (RAGE) and its ligands often leads to inflammatory processes or tissue injury, although the effect of the blockade of RAGE signaling on lung injury remains to be investigated. Objective: Using a murine model of lung injury induced by intratracheal lipopolysaccharide (LPS), we evaluated the RAGE expression in the airspace and the effect of recombinant soluble RAGE (sRAGE) on LPS-induced lung injury. Methods: First, the expression of sRAGE in bronchoalveolar lavage (BAL) fluid was determined at 24 h after intratracheal instillation of LPS or PBS. Next, to evaluate the effect of sRAGE, BAL fluid was collected for cell counting and measurements of lung permeability and cytokine concentrations 24 h after intratracheal LPS in the mice with or without intraperitoneal administration of sRAGE 1 h after the instillation. In another series, lungs were sampled for histopathology and detection of apoptotic cells. The activation of nuclear factor-{kappa}B (NF-{kappa}B) was analyzed 4 h after LPS instillation. Results: In response to LPS challenge, a RAGE isoform of 48 kD was detected in the BAL fluid. Treatment with sRAGE significantly attenuated the increases in neutrophil infiltration, lung permeability, production of inflammatory cytokines, NF-{kappa}B activation, and apoptotic cells in the lung as well as development of pathological changes after LPS instillation. Conclusion: RAGE plays an important role in the pathogenesis of LPS-induced lung injury in mice. Since blockade of RAGE signaling by sRAGE administered after LPS challenge was effective, it could be considered as a therapeutic modality.
Key words: RAGE, lung injury, apoptosis, chemokine, mouse model




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