Linked Life Data

18700232

Source:http://linkedlifedata.com/resource/pubmed/id/18700232

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-10-9
pubmed:abstractText
Increased levels of particulate matter have been associated with adverse effects in the respiratory as well as the cardiovascular system. The biological mechanisms behind these associations are still unresolved. Among potential mechanisms, particulate matter-associated cardiac effects may be initiated by inhaled small-sized particles, particle components and/or mediators related to inflammation that translocate into the pulmonary circulation. In the present study cytokine responses (interleukin [IL]-6, IL-1beta, and tumor necrosis factor [TNF]-alpha) of primary rat cardiomyocytes and cardiofibroblasts in mono- and cocultures induced by direct exposure to particles, were compared with cytokine responses induced by mediators released by particle-exposed primary rat epithelial lung cells (conditioned media). Cells were exposed to a model ultrafine particle (ultrafine carbon black, Printex 90) and in selected experiments to an urban air particle sample (SRM 1648, St Louis, MO). In lung cell cultures both particle types induced release of IL-6 and IL-1beta, whereas TNF-alpha was only detected upon exposure to St Louis particles. The release of IL-6 by cardiac cells was strongly enhanced upon exposure to conditioned media, and markedly exceeded the response to direct particle exposure. IL-1, but not TNF-alpha, seemed necessary, but not sufficient, for this enhanced IL-6 release. The role of IL-1 was demonstrated by use of an IL-1 receptor antagonist that partially reduced the effect of the conditioned media, and by a stimulating effect on the cardiac cell release of IL-6 by exogenous addition of IL-1alpha and IL-1beta. These in vitro findings lend support to the hypothesis that particle-induced cardiac inflammation and disease may involve lung-derived mediators.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1096-0929
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
106
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-41
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:18700232-Animals, pubmed-meshheading:18700232-Coculture Techniques, pubmed-meshheading:18700232-Culture Media, Conditioned, pubmed-meshheading:18700232-Cytokines, pubmed-meshheading:18700232-Dose-Response Relationship, Drug, pubmed-meshheading:18700232-Epithelial Cells, pubmed-meshheading:18700232-Fibroblasts, pubmed-meshheading:18700232-Inflammation Mediators, pubmed-meshheading:18700232-Interleukin-1beta, pubmed-meshheading:18700232-Interleukin-6, pubmed-meshheading:18700232-Lung, pubmed-meshheading:18700232-Male, pubmed-meshheading:18700232-Myocytes, Cardiac, pubmed-meshheading:18700232-Paracrine Communication, pubmed-meshheading:18700232-Particulate Matter, pubmed-meshheading:18700232-Rats, pubmed-meshheading:18700232-Rats, Inbred WKY, pubmed-meshheading:18700232-Soot, pubmed-meshheading:18700232-Tumor Necrosis Factor-alpha
pubmed:year
2008
pubmed:articleTitle
Particle-induced cytokine responses in cardiac cell cultures--the effect of particles versus soluble mediators released by particle-exposed lung cells.
pubmed:affiliation
Department of Air Pollution and Noise, Division of Environmental Medicine, Norwegian Institute of Public Health, NO-0403 Oslo, Norway. Annike.Irene.Totlandsdal@fhi.no
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't