Published ahead of print on April 14, 2005, doi:10.1164/rccm.200409-1174OC
Am. J. Respir. Crit. Care Med., Volume 172, Number 2, July 2005, 168-172
A more recent version of this article appeared on July 15, 2005
Submitted on September 7, 2004
Accepted on April 10, 2005
Short-term cigarette smoke exposure enhances allergic airway inflammation in mice
Katrien B Moerloose1*, Romain A Pauwels1, and Guy F Joos1
1 Department of Respiratory Diseases, Ghent University Hospital, Ghent, Belgium
* To whom correspondence should be addressed. E-mail: katrien.moerloose{at}UGent.be.
Rationale: Epidemiological studies suggest that tobacco smoke contributes to the prevalence
and occurrence of exacerbations in asthma. The effect of active smoking in adolescents with
atopy is poorly understood. Objectives: We developed an experimental model to investigate
the influence of smoking on antigen-induced airway inflammation and airway responsiveness
in mice that were previously sensitized. Methods: Ovalbumin (OVA)-sensitized BALB/c mice
were exposed to air or mainstream smoke (5 days a week) and to phosphate-buffered saline
(PBS) or OVA aerosol (3 times a week) for two weeks (n=8 for each group). Results: Airway
responsiveness to intravenously injected carbachol was increased (P<0.05) in smoke- and
OVA-exposed mice compared to all other groups. There was an additive effect of smoke and
OVA exposure on total cell numbers, macrophages and dendritic cells in bronchoalveolar
lavage fluid and on CD4- and CD8-positive T-lymphocytes and dendritic cells in lung tissue
(P<0.05 compared to mice exposed to smoke and PBS and to mice exposed to air and OVA).
Concurrent smoke- and OVA-exposure augmented OVA-specific immunoglobulin E in serum
compared to air- and OVA-exposure. In lavage fluid supernatant, eotaxin was increased in airand
OVA-exposed mice. The further increase observed in the group exposed to both OVA
and cigarette smoke came close to formal significance (P=0.06). TARC was augmented in
mice exposed to either smoke or ovalbumin, without additional effect. Conclusions: Our data
indicate that acute concurrent exposure to allergen and mainstream cigarette smoke enhances
airway inflammation and airway responsiveness in previously sensitized mice.
Key words: asthma, severity, additive, hyperreactivity, cytokines
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