PT - JOURNAL ARTICLE AU - L. Chen AU - B-B. Sun AU - T. Wang AU - X. Wang AU - J-Q. Li AU - H-X. Wang AU - S-F. Zhang AU - D-S. Liu AU - L. Liu AU - D. Xu AU - X-M. Ou AU - Y-J. Chen AU - T. Yang AU - H. Zhou AU - F-Q. Wen TI - Cigarette smoke enhances β-defensin 2 expression in rat airways <em>via</em> nuclear factor-κB activation AID - 10.1183/09031936.00029409 DP - 2010 Sep 01 TA - European Respiratory Journal PG - 638--645 VI - 36 IP - 3 4099 - http://erj.ersjournals.com/content/36/3/638.short 4100 - http://erj.ersjournals.com/content/36/3/638.full SO - Eur Respir J2010 Sep 01; 36 AB - β-defensin 2 (BD-2), an antimicrobial peptide, participates in airway defence. Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease. This study mainly aims to investigate the effect of CS on rat BD-2 (rBD-2) expression in rat airways. Rats were exposed to CS and treated with caffeic acid phenethyl ester (CAPE), a nuclear factor (NF)-κB inhibitor, or astragaloside IV (AS-IV), an active ingredient of Astragalus mongholicus. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes after CS exposure, rBD-2 expression was investigated with immunohistochemistry, reverse transcription PCR and ELISA. Total glutathione and nitric oxide (NO) levels in rat lungs were also detected. CS exposure markedly increased rBD-2 immunoreactivity, as well as rBD-2 mRNA and protein levels in rat airways, which were inhibited by CAPE treatment. Moreover, associated airway inflammation induced by CS was demonstrated by histological changes, increased cell counts and pro-inflammatory cytokines in BALF, and NF-κB activation and high levels of total glutathione and NO, which were all reversed by AS-IV in a dose-dependent fashion. In conclusion, CS exposure induces rBD-2 expression in rat airways via a NF-κB-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-κB inactivation.