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Short-term cigarette smoke exposure enhances allergic airway inflammation in mice

Katrien Moerloose UGent, Romain Pauwels and Guy Joos UGent (2005) AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. 172(2). p.168-172
abstract
Rationale: Epidemiologic 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 (S days/week) and to phosphate-buffered saline (PBS) or OVA aerosol (3 times/week) for 2 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 with 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(+) T lymphocytes and dendritic cells in lung tissue (p < 0.05 compared with mice exposed to smoke and PBS and to mice exposed to air and OVA). Concurrent smoke and OVA exposure augmented OVA-specific IgE in serum compared with air and OVA exposure. In lavage fluid supernatant, eotaxin was increased in air- and 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). Thymus- and activation-regulated chemokine was augmented in mice exposed to either smoke or OVA, 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.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
asthma, additive, cytokines, hyperresponsiveness, severity, CD8(+) T-CELLS, MURINE MODEL, LUNG DESTRUCTION, DENDRITIC CELLS, CHRONIC ASTHMA, MILD ASTHMA, HYPERRESPONSIVENESS, CHEMOKINE, ADULTS, SENSITIZATION
journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Am. J. Respir. Crit. Care Med.
volume
172
issue
2
pages
168-172 pages
Web of Science type
Article
Web of Science id
000230368400004
JCR category
RESPIRATORY SYSTEM
JCR impact factor
8.689 (2005)
JCR rank
1/33 (2005)
JCR quartile
1 (2005)
ISSN
1073-449X
DOI
10.1164/rccm.200409-1174OC
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
332299
handle
http://hdl.handle.net/1854/LU-332299
date created
2006-04-24 14:43:00
date last changed
2016-12-19 15:44:10
@article{332299,
  abstract     = {Rationale: Epidemiologic 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 (S days/week) and to phosphate-buffered saline (PBS) or OVA aerosol (3 times/week) for 2 weeks (n = 8 for each group). Results: Airway responsiveness to intravenously injected carbachol was increased (p {\textlangle} 0.05) in smoke- and OVA-exposed mice compared with 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(+) T lymphocytes and dendritic cells in lung tissue (p {\textlangle} 0.05 compared with mice exposed to smoke and PBS and to mice exposed to air and OVA). Concurrent smoke and OVA exposure augmented OVA-specific IgE in serum compared with air and OVA exposure. In lavage fluid supernatant, eotaxin was increased in air- and 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). Thymus- and activation-regulated chemokine was augmented in mice exposed to either smoke or OVA, 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.},
  author       = {Moerloose, Katrien and Pauwels, Romain and Joos, Guy},
  issn         = {1073-449X},
  journal      = {AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE},
  keyword      = {asthma,additive,cytokines,hyperresponsiveness,severity,CD8(+) T-CELLS,MURINE MODEL,LUNG DESTRUCTION,DENDRITIC CELLS,CHRONIC ASTHMA,MILD ASTHMA,HYPERRESPONSIVENESS,CHEMOKINE,ADULTS,SENSITIZATION},
  language     = {eng},
  number       = {2},
  pages        = {168--172},
  title        = {Short-term cigarette smoke exposure enhances allergic airway inflammation in mice},
  url          = {http://dx.doi.org/10.1164/rccm.200409-1174OC},
  volume       = {172},
  year         = {2005},
}

Chicago
Moerloose, Katrien, Romain Pauwels, and Guy Joos. 2005. “Short-term Cigarette Smoke Exposure Enhances Allergic Airway Inflammation in Mice.” American Journal of Respiratory and Critical Care Medicine 172 (2): 168–172.
APA
Moerloose, K., Pauwels, R., & Joos, G. (2005). Short-term cigarette smoke exposure enhances allergic airway inflammation in mice. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 172(2), 168–172.
Vancouver
1.
Moerloose K, Pauwels R, Joos G. Short-term cigarette smoke exposure enhances allergic airway inflammation in mice. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. 2005;172(2):168–72.
MLA
Moerloose, Katrien, Romain Pauwels, and Guy Joos. “Short-term Cigarette Smoke Exposure Enhances Allergic Airway Inflammation in Mice.” AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 172.2 (2005): 168–172. Print.