RT Journal Article SR Electronic T1 Increased expression of receptor for advanced glycation end products in COPD JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP P839 VO 44 IS Suppl 58 A1 Makoto Tanaka A1 Yoshimichi Ueda A1 Miyako Shimazaki A1 Masakatsu Ueno A1 Yuichiro Machida A1 Nozomu Motono A1 Katsuo Usuda A1 Motoyasu Sagawa A1 Tsutomu Sakuma YR 2014 UL http://erj.ersjournals.com/content/44/Suppl_58/P839.abstract AB Objective: COPD is a smoking-induced chronic inflammatory disease characterized with irreversible airway obstruction. Receptor for advanced glycation end products (RAGE) was found as a membranous receptor of advanced glycation end products in diabetic vascular damage, and has been revealed an important role in the initiation and amplification of chronic inflammation by binding multiple ligands. Lung is one of organs with constitutive high expression of RAGE. However, the pathological as well as physiological functions of RAGE in the lung have not been fully understood. Expression of RAGE in the lung of COPD was analyzed semi-quantitatively in order to elucidate its role in the pathogenesis and progression of COPD.Materials and methods: Formalin-fixed paraffin sections of lung tissues of 38 COPD and 37 non-COPD patients, obtained from the lung resection samples for lung cancer, were immunostained with anti-RAGE antibody. The signal intensity of RAGE (RAGE-SI) in type 1 alveolar cells (ATI), bronchiolar cells and alveolar macrophage (AM) was analyzed morphometrically and evaluated relationship with clinic-pathologic factors.Results: RAGE-SI of ATI and AM were significantly increased in COPD group compared with those in non-COPD group. Those RAGE-SI correlated negatively with FEV1. RAGE expression was not associated with smoking index.Conclusion: These results showed the enhanced expression of RAGE in COPD lung and involvement of RAGE in the progression of obstructive gas exchange, suggesting that RAGE may be a promising target for the control of COPD. Expression of RAGE in alveoli of COPD lung is stimulated not directly by smoking but indirectly through chronic inflammation-related pathways.