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Thorax 2009;64:144-149 doi:10.1136/thx.2008.102681
  • Airway biology

Suppression of pulmonary innate host defence in smokers

  1. C Herr1,
  2. C Beisswenger1,
  3. C Hess1,
  4. K Kandler1,
  5. N Suttorp2,
  6. T Welte3,
  7. J-M Schroeder4,
  8. C Vogelmeier1,
  9. R Bals for the CAPNETZ Study Group1
  1. 1
    Department of Internal Medicine, Division for Pulmonary Diseases, Philipps-Universtät Marburg, Marburg, Germany
  2. 2
    Department of Internal Medicine/Infectious Diseases, Charité, Universitätsmedizin, Berlin, Germany
  3. 3
    Department of Internal Medicine, Division for Pulmonary Diseases, Medizinische Hochschule Hannover, Hanover, Germany
  4. 4
    Clinical Research Unit at the Department of Dermatology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany
  1. Professor R Bals, Department of Internal Medicine, Division of Pulmonology, Hospital of the University of Marburg, Baldingerstrasse 1, 35043 Marburg, Germany; bals{at}mailer.uni-marburg.de
  • Received 4 June 2008
  • Accepted 23 September 2008
  • Published Online First 13 October 2008

Abstract

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

Methods: Using sensitive ex vivo analysis, the level of the endogenous antibiotic peptide human β-defensin-2 (hBD-2) was measured in pharyngeal washing fluid and sputum from patients with community acquired pneumonia. The regulation of antibacterial host defence molecules was studied in vitro. The effect of cigarette smoke on the antibacterial activity of differentiated airway epithelium and the expression of host defence molecules was studied in an in vitro infection model.

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 hydrogen peroxide, and catalase blunted the smoke-induced inhibition of epithelial host defence.

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

Footnotes

  • Funding: Supported by grants from the Deutsche Forschungsgemeinschaft (Ba 1641/8-1;SBF/TR 22) to RB and from the German Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung, BMBF) via CAPNETZ to RB (01KI0432), NS (01KI0426) and TW (01KI0429).

  • Competing interests: None.

  • Ethics approval: The study was approved by local ethics committees and informed consent was obtained from the patients.

This Article

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  4. All versions of this article:
    1. thx.2008.102681v1
    2. 64/2/144 most recent

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