Emphysema requires the receptor for advanced glycation end-products triggering on structural cells.

Published on Apr 1, 2015in American Journal of Respiratory Cell and Molecular Biology5.373
· DOI :10.1165/RCMB.2014-0027OC
Koichi Waseda9
Estimated H-index: 9
(Okayama University),
Nobuaki Miyahara33
Estimated H-index: 33
(RMIT: RMIT University)
+ 9 AuthorsArihiko Kanehiro25
Estimated H-index: 25
Sources
Abstract
Pulmonary emphysema is characterized by persistent inflammation and progressive alveolar destruction. The receptor for advanced glycation end-products (RAGE) is a multiligand cell surface receptor reported to be involved in the process of acute alveolar epithelial cell injury. However, studies that address the role of RAGE in pulmonary emphysema are inconclusive. We investigated the role of RAGE in the development of elastase-induced pulmonary inflammation and emphysema in mice. RAGE-sufficient (RAGE+/+) mice and RAGE-deficient (RAGE−/−) mice were treated with intratracheal elastase on Day 0. Airway inflammation, static lung compliance, lung histology, and the levels of neutrophil-related chemokine and proinflammatory cytokines in bronchoalveolar lavage fluid were determined on Days 4 and 21. Neutrophilia in bronchoalveolar lavage fluid, seen in elastase-treated RAGE+/+ mice, was reduced in elastase-treated RAGE−/− mice on Day 4, and was associated with decreased levels of keratinocyte chemoattractant, ma...
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