@article {NabeP3341, author = {Takeshi Nabe and Tomohiko Sekioka and Michiaki Kadode and Masanori Fujii and Takashi Abe and Michiaki Horiba and Shigekatsu Kohno and Kazuhito Kawabata}, title = {Expression of CysLT2 receptors in asthmatic lung, and the roles in bronchoconstriction}, volume = {44}, number = {Suppl 58}, elocation-id = {P3341}, year = {2014}, publisher = {European Respiratory Society}, abstract = {Background: Expression and functional roles of CysLT2 receptors in asthmatic airways have been unclear.Objectives: Expression of both CysLT1 and CysLT2 receptors in the lung of asthma patients, and their functional roles in antigen-induced bronchial contraction were comparatively examined, and they were compared with those of non-asthma subjects.Methods: Expression of CysLT1 and CysLT2 receptors in the airway tissues isolated from asthma and non-asthma subjects were assessed by immunohistochemistry. As assessment of the functional roles, effects of a CysLT2 receptor-specific antagonist, BayCysLT2RA, and a dual CysLT1/2 receptor antagonist, ONO-6950 on antigen-induced bronchial contraction were evaluated in vitro.Results: Both CysLT1 and CysLT2 receptors were expressed on the smooth muscle and the epithelium of the bronchi, and alveolar leukocytes. Relative expression of CysLT2 receptors to CysLT1 receptors especially in the smooth muscle of the asthmatic lung showed a tendency to be higher than that in non-asthma subjects. CysLT2 receptor-blockade hardly potentiated an inhibitory effect of a CysLT1-specific antagonist, montelukast, on the antigen-induced contraction of bronchi of non-asthma subjects. However, in the bronchus from one of 2 asthma patients, CysLT2 receptor antagonism suppressed the contraction, and both CysLT1 and CysLT2 receptor blockade showed additive inhibitory effects on the anaphylactic contraction.Conclusions: CysLT2 receptor activation by cysteinyl leukotrienes may play roles in a certain asthma patient, suggesting that CysLT2 receptor antagonists and dual CysLT1/2 receptor antagonists could be new therapeutic agents for asthma.}, issn = {0903-1936}, URL = {https://erj.ersjournals.com/content/44/Suppl_58/P3341}, eprint = {https://erj.ersjournals.com/content}, journal = {European Respiratory Journal} }