Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-8-27
pubmed:abstractText
In this study we investigated the alterations in protein levels that are induced by allergic eosinophilic lung inflammation. Lung tissue eosinophilia and sequestration of inflammatory cells in airspaces were provoked by systemic sensitization with ovalbumin followed by repeated inhalation challenge with aerosolized ovalbumin. Proteome alterations in lung tissue and bronchoalveolar lavage fluid, respectively, were examined by two-dimensional gel electrophoresis followed by identification of proteins by mass spectrometry. Several proteins were markedly increased in inflamed tissue. In particular, several proteins that are known to be associated with hypoxia were elevated, for example, glycolytic enzymes, glucose-regulated protein 78 kD, prolyl-4-hydroxylase, peroxiredoxin 1, and arginase. Out of the identified proteins, Ym2 displayed the clearest increase, present at high levels in animals with lung eosinophilia, while being undetectable in control subjects. Furthermore, the levels of cathepsin S were markedly increased in inflamed tissue. Taken together, this study identifies a number of marker proteins associated with the pathogenesis of allergic lung inflammation and indicates a link between allergic airway inflammation and induction of hypoxia-related gene products.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
170
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
477-84
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Increased levels of hypoxia-sensitive proteins in allergic airway inflammation.
pubmed:affiliation
Swedish University of Agricultural Sciences, Department of Molecular Biosciences, The Biomedical Centre, Box 575, 75123 Uppsala, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't