Short-term smoke exposure attenuates ovalbumin-induced airway inflammation in allergic mice

Am J Respir Cell Mol Biol. 2004 Jun;30(6):880-5. doi: 10.1165/rcmb.2003-0178OC. Epub 2004 Jan 12.


Little is known about effects of smoking on airway inflammation in asthma. We tested the hypothesis that smoking enhances established airway inflammation in a mouse model of allergic asthma. C57Bl/6j mice were sensitized to ovalbumin (OVA) and challenged with OVA (OVA-mice) or sham-sensitized to phosphate-buffered saline (PBS) and challenged with PBS aerosols (PBS-mice) for 7 wk. At 4 wk, mice were additionally exposed to air (nonsmoking controls) or mainstream smoke for 3 wk. Using whole body plethysmography, we found OVA-induced bronchoconstriction to be significantly inhibited in smoking OVA-mice as compared with nonsmoking OVA-mice (1 +/- 2% increase versus 22 +/- 6% increase in enhanced pause, respectively). Smoking did not change airway hyperresponsiveness (AHR) to methacholine in PBS-mice, yet significantly attenuated AHR in OVA-mice 24 h after OVA challenge as compared with nonsmoking mice. This was accompanied by reduced eosinophil numbers in lung lavage fluid and tissue of smoking OVA-mice compared with nonsmoking OVA-mice. In contrast to our hypothesis, short-term smoking reduced responsiveness to OVA and methacholine in OVA-mice and decreased airway inflammation when compared with nonsmoking mice. This effect of smoking may be different for long-term smoking, in which remodeling effects of smoking can be expected to interrelate with remodeling changes caused by asthmatic disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Inhalation
  • Air Pollutants
  • Animals
  • Asthma / chemically induced
  • Asthma / immunology*
  • Asthma / metabolism
  • Bronchial Hyperreactivity*
  • Bronchial Provocation Tests
  • Bronchoalveolar Lavage Fluid / chemistry
  • Bronchoalveolar Lavage Fluid / cytology
  • Bronchoconstriction / physiology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Inflammation / chemically induced*
  • Lung / cytology
  • Lung / immunology
  • Lung / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / immunology*
  • Plethysmography, Whole Body
  • Smoke*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Time Factors


  • Air Pollutants
  • Cytokines
  • Smoke
  • Ovalbumin