Published ahead of print on January 12, 2004, doi:10.1165/rcmb.2003-0178OC
Am. J. Respir. Cell Mol. Biol., Volume 30, Number 6, June 2004, 880-885
A more recent version of this article appeared on June 1, 2004
Submitted on May 6, 2003
Revised on January 7, 2004
Short-term smoke exposure attenuates ovalbumin-induced airway inflammation in allergic mice
Barbro N Melgert1*, Dirkje S Postma2, Marie Geerlings1, Marjan A Luinge1, Pieter A Klok3, Barry W.A. van der Strate1, Huib A.M. A Kerstjens2, Wim Timens3, and Machteld N Hylkema3
1 Department of Pathology and Laboratory Medicine, University Hospital Groningen, Groningen, The Netherlands; Department of Pulmonology, University Hospital Groningen, Groningen, The Netherlands,
2 Department of Pulmonology, University Hospital Groningen, Groningen, The Netherlands,
3 Department of Pathology and Laboratory Medicine, University Hospital Groningen, Groningen, The Netherlands
* To whom correspondence should be addressed. E-mail: b.n.melgert{at}path.azg.nl.
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 PBS and challenged with PBS aerosols (PBS-mice) for 7 weeks. At 4 weeks, mice were additionally exposed to air (nonsmoking controls) or mainstream smoke for 3 weeks. Using whole body plethysmography we found OVA-induced bronchoconstriction to be significantly inhibited in smoking OVA-mice as compared to nonsmoking OVA-mice (1±2% increase vs. 22±6% increase in Penh, respectively). Smoking did not change airway hyperresponsiveness (AHR) to methacholine in PBS-mice, yet significantly attenuated AHR in OVA-mice 24 hours after OVA-challenge as compared to nonsmoking mice. This was accompanied by reduced eosinophil numbers in lung lavage fluid and tissue of smoking OVA-mice compared to 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 to 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.
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