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Airway bacterial infections pose a significant challenge to the management of COPD, a disease mainly caused by cigarette smoking. However, the mechanisms of impaired airway mucosal innate immunity against bacteria in COPD remain unclear. We examined the effect of cigarette smoke on prostaglandin E2 (PGE2) and downstream epithelial host defence mechanisms including the antimicrobial substance human β-defensin-2 (hBD-2).Brushed bronchial epithelial cells were obtained from healthy smokers and individuals with COPD, and cultured under air–liquid interface conditions with or without exposure to whole cigarette smoke (WCS) or Moraxella catarrhalis (Mc) infection. Bacterial load, hBD-2 (a molecule known to kill Mc) and PGE2 were measured.WCS decreased Mc-induced hBD-2 expression and increased Mc load on bronchial epithelial cells from healthy smokers and COPD patients. Moreover, WCS inhibited PGE2 induction following Mc. PGE2 was shown to increase hBD-2 production in bronchial epithelial cells from healthy smokers, but not from COPD patients.The results suggest that in well-differentiated human bronchial epithelial cells, WCS may impair host defence against Mc in part through inhibiting PGE2 production.We determined the impact of cigarette smoke on cultured human (smokers and COPD patients) bronchial epithelial cell innate immune response to Moraxella catarrhalis infection. Cigarette smoke increased bacterial load, but decreased prostaglandin E2 (PGE2). Furthermore, PGE2 directly enhanced the production of human β-defensin-2, a well-known bactericidal molecule. Our results help clarify the role of PGE2 in mucosal innate immunity of COPD patients.