Linked Life Data

19085563

Source:http://linkedlifedata.com/resource/pubmed/id/19085563

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-12-16
pubmed:abstractText
Chronic obstructive pulmonary diseases (COPD) may increase air pollution-related mortality. The relationship of immune mechanisms to mortality caused by fine particulates in healthy and COPD populations is incompletely understood. The objective of this study was to determine whether fine particulates from a single biomass fuel alter stress and inflammation biomarkers in people with COPD. Healthy and COPD subjects were exposed to smoke in a controlled indoor setting. Immune responses were quantified by measuring cell surface marker expression with flow-cytometric analysis and mRNA levels with quantitative reverse transcriptase-polymerase chain reactions in whole blood before and after exposure. Preexposure COPD subjects had more leukocytes, mainly CD14(+) monocytes and neutrophils, but fewer CD3(+) T cells. Fifty-seven of 186 genes were differentially expressed between healthy and COPD subjects' peripheral blood mononuclear cells (PBMCs). Of these, only nuclear factor (NF)-kappa B1, TIMP-1, TIMP-2, and Duffy genes were up-regulated in COPD subjects. At 4 hours post smoke exposure, monocyte levels decreased only in healthy subjects. Fifteen genes, particular to inflammation, immune response, and cell-to-cell signaling, were differentially expressed in COPD subjects, versus 4 genes in healthy subjects. The authors observed significant differences in subjects' PBMCs, which may elucidate the adverse effects of air pollution particulates on people with COPD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1521-0499
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
631-62
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Enhanced acute responses in an experimental exposure model to biomass smoke inhalation in chronic obstructive pulmonary disease.
pubmed:affiliation
Department of Experimental Pathology and Pharmacology, Schering-Plough Biopharma, Palo Alto, California, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't