Linked Life Data

7767546

Source:http://linkedlifedata.com/resource/pubmed/id/7767546

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1995-6-30
pubmed:abstractText
Idiopathic pulmonary fibrosis (IPF) is a poorly understood interstitial disease that usually proves refractory to therapy and results in irreversible tissue scarring and pulmonary dysfunction. Previous investigations have suggested a number of possible mediators of inflammation and fibrosis that typify IPF. We report increases in lung interleukin-1 receptor antagonist protein (IRAP) content in patients with IPF, as compared with normal control subjects. Importantly, this increase in IRAP was not accompanied by concomitant increases in interleukin-1 beta (IL-1 beta), resulting in a local environment that may be profibrotic. Tissue homogenates and bronchoalveolar lavage fluid from patients with IPF both demonstrate elevated IRAP content compared with that in normal subjects. Immunohistochemical staining and in situ hybridization localize IRAP to hyperplastic type II pneumocytes, macrophages, and local stromal cells. Finally, in vitro studies utilizing fibroblasts isolated from patients with IPF demonstrated no difference in constitutive IRAP production compared with that in normal subjects, but they revealed an exaggerated response to stimulation with transforming growth factor-beta (TGF-beta). These findings suggest that the fibrotic tissue changes of IPF and possibly other chronic interstitial lung diseases may result in part from the local effects of IRAP, and they also demonstrate that pulmonary nonimmune cells may influence local tissue changes through the elaboration of IRAP.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
1965-73
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7767546-Bronchoalveolar Lavage Fluid, pubmed-meshheading:7767546-Case-Control Studies, pubmed-meshheading:7767546-Female, pubmed-meshheading:7767546-Fibroblasts, pubmed-meshheading:7767546-Gene Expression, pubmed-meshheading:7767546-Humans, pubmed-meshheading:7767546-Immunohistochemistry, pubmed-meshheading:7767546-In Situ Hybridization, pubmed-meshheading:7767546-Interleukin 1 Receptor Antagonist Protein, pubmed-meshheading:7767546-Interleukin-1, pubmed-meshheading:7767546-Lung, pubmed-meshheading:7767546-Male, pubmed-meshheading:7767546-Middle Aged, pubmed-meshheading:7767546-Pulmonary Fibrosis, pubmed-meshheading:7767546-RNA, Messenger, pubmed-meshheading:7767546-Receptors, Interleukin-1, pubmed-meshheading:7767546-Sialoglycoproteins, pubmed-meshheading:7767546-Transforming Growth Factor beta, pubmed-meshheading:7767546-Tumor Necrosis Factor-alpha
pubmed:year
1995
pubmed:articleTitle
Increased interleukin-1 receptor antagonist in idiopathic pulmonary fibrosis. A compartmental analysis.
pubmed:affiliation
Department of Medicine, University of Michigan Medical School, Ann Arbor, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.