Linked Life Data

12817015

Source:http://linkedlifedata.com/resource/pubmed/id/12817015

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-6-20
pubmed:abstractText
Adenosine-induced bronchoconstriction is a well-recognized feature of atopic asthma. Adenosine acts through four different G protein-coupled receptors to produce a myriad of physiological effects. To examine the contribution of the A(3) adenosine receptor to adenosine-induced bronchoconstriction and to assess the contribution of mast cells to this process, we quantified airway responsiveness to aerosolized adenosine in wild-type, A(3) receptor-deficient, and mast cell-deficient mice. Compared with the robust airway responses elicited by adenosine in wild-type mice, both A(3)-deficient and mast cell-deficient mice exhibited a significantly attenuated response compared with their respective wild-type controls. Histological examination of the airways 4 h after adenosine exposure revealed extensive degranulation of airway mast cells as well as infiltration of neutrophils in wild-type mice, whereas these findings were much diminished in A(3)-deficient mice and were not different from those in PBS-treated controls. These data indicate that the airway responses to aerosolized adenosine in mice occur largely through A(3) receptor activation and that mast cells contribute significantly to these responses, but that activation of additional adenosine receptors on a cell type(s) other than mast cells also contributes to adenosine-induced airway responsiveness in mice. Finally, our findings indicate that adenosine exposure can result in A(3)-dependent airway inflammation, as reflected in neutrophil recruitment, as well as alterations in airway function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
171
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
331-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12817015-Adenosine, pubmed-meshheading:12817015-Administration, Inhalation, pubmed-meshheading:12817015-Aerosols, pubmed-meshheading:12817015-Animals, pubmed-meshheading:12817015-Bronchial Hyperreactivity, pubmed-meshheading:12817015-Cell Degranulation, pubmed-meshheading:12817015-Down-Regulation, pubmed-meshheading:12817015-Inflammation, pubmed-meshheading:12817015-Lung, pubmed-meshheading:12817015-Mast Cells, pubmed-meshheading:12817015-Mice, pubmed-meshheading:12817015-Mice, Inbred C57BL, pubmed-meshheading:12817015-Mice, Knockout, pubmed-meshheading:12817015-Mice, Mutant Strains, pubmed-meshheading:12817015-Neutrophil Infiltration, pubmed-meshheading:12817015-Receptor, Adenosine A3, pubmed-meshheading:12817015-Receptors, Purinergic P1, pubmed-meshheading:12817015-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
Identification of A3 receptor- and mast cell-dependent and -independent components of adenosine-mediated airway responsiveness in mice.
pubmed:affiliation
Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.