PT - JOURNAL ARTICLE AU - Utako Fujii AU - Nobuaki Miyahara AU - Akihiko Taniguchi AU - Daisuke Morichika AU - Naohiro Oda AU - Koichi Waseda AU - Etsuko Kurimoto AU - Mikio Kataoka AU - Akihiko Yoshimura AU - Arihiko Kanehiro AU - Mitsune Tanimoto TI - IL-23 is essential to the development of elastase-induced pulmonary inflammation and emphysema AID - 10.1183/13993003.congress-2016.PA1831 DP - 2016 Sep 01 TA - European Respiratory Journal PG - PA1831 VI - 48 IP - suppl 60 4099 - http://erj.ersjournals.com/content/48/suppl_60/PA1831.short 4100 - http://erj.ersjournals.com/content/48/suppl_60/PA1831.full SO - Eur Respir J2016 Sep 01; 48 AB - RATIONALE: We have recently reported that IL-17A plays a critical role to the development of porcine pancreatic elastase (PPE)-induced emphysema. The proliferation of Th17 cells is induced by IL-23, however, the role of IL-23 in pulmonary emphysema remains uncertain.METHODS: Using a murine model of PPE-induced pulmonary emphysema, we assessed IL-23p19-deficient (IL-23-/-) mice and wild type (WT) mice. Intra-tracheal instillation of PPE induced increased emphysematous change of the lungs on day 21, associated with increased levels of IL-23 in lung homogenates.RESULT: IL-23-/- mice developed significantly lower static compliance values and decreased emphysematous changes in the lung tissue compared to WT mice on day 21 after PPE-instillation, associated with lower levels of IL-17 and lower numbers of Th17 cells in the lung.CONCLUSION: These data identify the important contribution of IL-23 to the development of elastase-induced pulmonary inflammation and emphysema probably through IL-23-IL-17 pathway. Targeting IL-23 in emphysema is a potential therapeutic strategy for delaying disease progression.