Linked Life Data

9379061

Source:http://linkedlifedata.com/resource/pubmed/id/9379061

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1997-11-12
pubmed:abstractText
Presently, there is considerable evidence for the participation of eosinophils in the pathophysiology of human bronchial asthma. Although increased numbers of eosinophils are present in the airways and bronchoalveolar lavage (BAL) fluid of atopic asthmatics, the mechanisms responsible for their preferential accumulation are still largely unknown. Eotaxin is a chemokine that promotes the selective recruitment of eosinophils. We report that atopic asthmatic patients have high concentrations of eotaxin in BAL fluid and an increased expression of eotaxin mRNA and protein in the epithelium and submucosa of their airways when compared with normal controls. In the BAL cells from asthmatic patients, eotaxin immunoreactivity colocalized predominantly to macrophages (62.2%), with a lesser contribution from T cells (16.3%) and eosinophils (8.9%). BAL fluid from asthmatics contained chemotactic activity for eosinophils that was attributable in part to the presence of eotaxin. Moreover, eotaxin was more effective at inducing in vitro eosinophil chemotaxis when eosinophils were stimulated with IL-5 (a cytokine that enhances the effector capacity of mature eosinophils). These observations suggest that eotaxin contributes to the pathogenesis of asthma by the specific recruitment of eosinophils into the airways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4593-601
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Increased expression of eotaxin in bronchoalveolar lavage and airways of asthmatics contributes to the chemotaxis of eosinophils to the site of inflammation.
pubmed:affiliation
Department of Medicine, McGill University, Montreal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't