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Suppression of pulmonary innate host defense in smokers
  1. Christian Herr (herrc{at}staff.uni-marburg.de)
  1. University of Marburg, Germany
    1. Kerstin Kandler (kiki2{at}gmx.net)
    1. University of Marburg, Germany
      1. Christoph Beisswenger (beisswen{at}mail.med.upenn.edu)
      1. University of Marburg, Germany
        1. Christian Hess (chester1{at}web.de)
        1. University of Marburg, Germany
          1. Norbert Suttorp (norbert.suttorp{at}charite.de)
          1. Charité Universitätsmedizin Berlin, Germany
            1. Tobias Welte (welte.tobias{at}mh-hannover.de)
            1. Medizinische Hochschule Hannover, Germany
              1. Jens-Michel Schröder (jschroeder{at}dermatology.uni-kiel.de)
              1. University of Kiel, Germany
                1. Claus Vogelmieir (claus.vogelmeier{at}med.uni-marburg.de)
                1. Marburg University, Germany
                  1. Robert Bals (bals{at}staff.uni-marburg.de)
                  1. University of Marburg, Germany

                    Abstract

                    Background: Smoking increases the susceptibility to pulmonary infection and is a risk factor for the development of chronic obstructive pulmonary disease (COPD). We postulated that cigarette smoke suppresses the activation of the innate immune system in response to bacterial infection.

                    Methods: With sensitive ex-vivo analysis we measured the level of the endogenous antibiotic peptide human beta-defensin-2 in pharyngeal washing fluids and sputum of patients with community acquired pneumonia. The regulation of antibacterial host defense molecules was studied in vitro. The effect of cigarette smoke on the antibacterial activity of differentiated airway epithelium and the expression of host defense molecules was studied in an infection model in vitro.

                    Results: Current or former smoking was associated with significantly reduced hBD-2 levels in pharyngeal washing fluid and sputum from patients with acute pneumonia. Exposure of airway epithelium to smoke in vitro inhibited the induction of hBD-2 by bacteria. This correlated with decreased antimicrobial activity. This effect was mimicked by H2O2 and catalase blunted the smoke-induced inhibition of epithelial host defense.

                    Conclusions: Smoke exposure suppresses the induction of epithelial antibacterial host defenses. These findings link smoking with increased susceptibility to infection. This mechanism may be important in the pathogenesis of pneumonia and COPD.

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