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

*Bijbehorende auteur voor dit werk

OnderzoeksoutputAcademicpeer review

84 Citaten (Scopus)


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.

Originele taal-2English
Pagina's (van-tot)880-885
Aantal pagina's6
TijdschriftAmerican Journal of Respiratory Cell and Molecular Biology
Nummer van het tijdschrift6
StatusPublished - jun-2004

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