Contrasting roles for the receptor for advanced glycation end-products on structural cells in allergic airway inflammation vs. Airway hyperresponsiveness

Published on Oct 15, 2015in American Journal of Physiology-lung Cellular and Molecular Physiology4.406
· DOI :10.1152/AJPLUNG.00087.2015
Akihiko Taniguchi10
Estimated H-index: 10
(Okayama University),
Nobuaki Miyahara33
Estimated H-index: 33
(RMIT: RMIT University)
+ 9 AuthorsArihiko Kanehiro25
Estimated H-index: 25
(Okayama University)
Sources
Abstract
The receptor for advanced glycation end-products (RAGE) is a multiligand receptor that belongs to the immunoglobulin superfamily. RAGE is reported to be involved in various inflammatory disorders; however, studies that address the role of RAGE in allergic airway disease are inconclusive. RAGE-sufficient (RAGE+/+) and RAGE-deficient (RAGE−/−) mice were sensitized to ovalbumin, and airway responses were monitored after ovalbumin challenge. RAGE−/− mice showed reduced eosinophilic inflammation and goblet cell metaplasia, lower T helper type 2 (Th2) cytokine production from spleen and peribronchial lymph node mononuclear cells, and lower numbers of group 2 innate lymphoid cells in the lung compared with RAGE+/+ mice following sensitization and challenge. Experiments using irradiated, chimeric mice showed that the mice expressing RAGE on radio-resistant structural cells but not hematopoietic cells developed allergic airway inflammation; however, the mice expressing RAGE on hematopoietic cells but not structura...
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