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

BN Melgert*, DS Postma, M Geerlings, MA Luinge, PA Klok, BWA van der Strate, HAM Kerstjens, W Timens, MN Hylkema

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

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.

Original languageEnglish
Pages (from-to)880-885
Number of pages6
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume30
Issue number6
DOIs
Publication statusPublished - Jun-2004

Keywords

  • EOSINOPHIL INFILTRATION
  • PULMONARY EOSINOPHILIA
  • INCREASED EXPRESSION
  • LUNG-FUNCTION
  • YOUNG-ADULTS
  • MURINE MODEL
  • MOUSE MODEL
  • ASTHMA
  • HYPERRESPONSIVENESS
  • CELL

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