Cigarette smoke enhances {beta}-defensin 2 expression in rat airways via nuclear factor-{kappa}B activation / L. Chen (2010)  

Public Titre : Cigarette smoke enhances {beta}-defensin 2 expression in rat airways via nuclear factor-{kappa}B activation Type de document : texte imprimé Auteurs : L. Chen, Auteur ; P.P. Sun, Auteur ; T. Wang, Auteur ; X. Wang, Auteur Editeur : European Respiratory Society (ERS) Année de publication : 2010 Collection : European Respiratory Journal num. 36 Importance : p.638-645 Présentation : graph., ill. Langues : Anglais (eng) Catégories : [TABAC] chimie du tabac:fumée [TABAC] étude [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive Index. décimale : TA 3.2.2.1 Expérimentation Résumé : 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. En ligne : https://erj.ersjournals.com/content/36/3/638.long Permalink : https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8075

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