Linked Life Data

21317378

Source:http://linkedlifedata.com/resource/pubmed/id/21317378

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-10-5
pubmed:abstractText
Although a similar prevalence of smoking is evident among patients with asthma and the general population, little is known about the impact of cigarette smoke on the immune inflammatory processes elicited by common environmental allergens. We investigated the impact of exposure to cigarette smoke on house dust mite (HDM)-induced allergic airway inflammation and its consequences for tissue remodeling and lung physiology in mice. BALB/c mice received intranasal HDMs daily, 5 days per week, for 3 weeks to establish chronic airway inflammation. Subsequently, mice were concurrently exposed to HDMs plus cigarette smoke, 5 days per week, for 2 weeks (HDMs + smoke). We observed significantly attenuated eosinophilia in the bronchoalveolar lavage of mice exposed to HDMs + smoke, compared with animals exposed only to HDMs. A similar activation of CD4 T cells and expression of IL-5, IL-13, and transforming growth factor-? was observed between HDM-treated and HDM + smoke-treated animals. Consistent with an effect on eosinophil trafficking, HDMs + smoke exposure attenuated the HDM-induced expression of eotaxin-1 and vascular cell adhesion molecule-1, whereas the survival of eosinophils and the numbers of blood eosinophils were not affected. Exposure to cigarette smoke also reduced the activation of B cells and the concentrations of serum IgE. Although the production of mucus decreased, collagen deposition significantly increased in animals exposed to HDMs + smoke, compared with animals exposed only to HDMs. Although airway resistance was unaffected, tissue resistance was significantly decreased in mice exposed to HDMs + smoke. Our findings demonstrate that cigarette smoke affects eosinophil migration without affecting airway resistance or modifying Th2 cell adaptive immunity in a murine model of HDM-induced asthma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1535-4989
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
753-60
pubmed:meshHeading
pubmed-meshheading:21317378-Airway Remodeling, pubmed-meshheading:21317378-Airway Resistance, pubmed-meshheading:21317378-Allergens, pubmed-meshheading:21317378-Animals, pubmed-meshheading:21317378-Asthma, pubmed-meshheading:21317378-B-Lymphocytes, pubmed-meshheading:21317378-Bronchial Hyperreactivity, pubmed-meshheading:21317378-Chemokine CCL11, pubmed-meshheading:21317378-Dendritic Cells, pubmed-meshheading:21317378-Disease Models, Animal, pubmed-meshheading:21317378-Female, pubmed-meshheading:21317378-Interleukin-13, pubmed-meshheading:21317378-Interleukin-5, pubmed-meshheading:21317378-Lung, pubmed-meshheading:21317378-Mice, pubmed-meshheading:21317378-Mice, Inbred BALB C, pubmed-meshheading:21317378-Pulmonary Eosinophilia, pubmed-meshheading:21317378-Pyroglyphidae, pubmed-meshheading:21317378-Smoking, pubmed-meshheading:21317378-T-Lymphocytes, pubmed-meshheading:21317378-Time Factors, pubmed-meshheading:21317378-Transforming Growth Factor beta, pubmed-meshheading:21317378-Vascular Cell Adhesion Molecule-1
pubmed:year
2011
pubmed:articleTitle
Cigarette smoke differentially affects eosinophilia and remodeling in a model of house dust mite asthma.
pubmed:affiliation
Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5 Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't