Linked Life Data

7713208

Source:http://linkedlifedata.com/resource/pubmed/id/7713208

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1995-5-15
pubmed:abstractText
Histopathological studies of asthmatic airways removed postmortem or by bronchial biopsy show marked inflammatory changes, notably epithelial cell disruption and damage, and the presence of large numbers of eosinophils. The epithelial damage is seen in mild, asymptomatic asthmatics as well as in patients who have died in status asthmaticus. Damage to the epithelium may also correlate with bronchial hyperreactivity. The epithelium has been suggested to be a target for inflammatory cell mediators and cytokines. Recently, the airway epithelium has itself been shown to produce and release several proinflammatory mediators and cytokines, and to express adhesion molecules for inflammatory cells. The epithelium, thus, may actively participate in the inflammatory changes in asthma, where it may be a source as well as a target. Drug therapy aimed at preventing inflammatory changes in the epithelium, such as cytokine and adhesion molecule expression, may be an important step forward in halting disease progression in asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0903-1936
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2226-33
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Proinflammatory potential of the airway epithelium in bronchial asthma.
pubmed:affiliation
Rhône-Poulenc Rorer, Ltd, Dagenham Research Centre, Essex, UK.
pubmed:publicationType
Journal Article, Review