Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-5-23
pubmed:abstractText
Asthmatic patients show an increased expression of inducible nitric oxide synthase (iNOS) in airway epithelial cells and an increased level of nitric oxide (NO) in exhaled air. The NO derived from airway epithelial cells may be a mechanism for amplifying and perpetuating asthmatic inflammation, through inhibition of T helper 1 (Th1) cells and their production of interferon gamma (IFN-gamma). This would result in an increase in the number of Th2 cells and the cytokines interleukin 4 (IL-4) (which is important for IgE expression) and IL-5 (which plays a critical role in the recruitment of eosinophils into the airways). Although this mechanism may be part of our nonspecific airway defence against parasite invasion, it appears to have been activated inappropriately in asthma. Here, Peter Barnes and Eddy Liew argue that the development of specific iNOS inhibitors may represent a novel therapeutic approach for asthma and other allergic diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0167-5699
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Nitric oxide and asthmatic inflammation.
pubmed:affiliation
Dept of Thoracic Medicine, National Heart and Lung Institute, London, UK.
pubmed:publicationType
Journal Article, Review