Linked Life Data

8048050

Source:http://linkedlifedata.com/resource/pubmed/id/8048050

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-8-30
pubmed:abstractText
Inhalation of ozone (O3) has been associated with development of inflammation in the respiratory airways and a variety of alterations in pulmonary function. Epithelial cells lining the airways are the first cells with which inhaled O3 comes into contact and thus represent a potential major target of acute O3 toxicity. In addition, upon appropriate stimulation or injury, these cells are capable of releasing a spectrum of secondary mediators that could relate to the pathogenesis of O3-associated lesions. We exposed organotypically cultured guinea pig primary tracheal epithelial (GPTE) cells in an air/liquid interface to photochemically generated O3 in vitro and monitored effects of O3 exposure on activation of phospholipases A2 (PLA2), C (PLC), and D (PLD), as well as release of the humoral mediator, platelet activating factor (PAF). PLA2 acts on ether-linked phosphatidylcholine, which upon further metabolism forms PAF;PLC acts on inositol phospholipids to produce inositol phosphates and diacylglycerol; and PLD generates phosphatidic acid. GPTE cell cultures exposed to O3 (0.05-1.0 ppm) for 1 hr displayed an elevated total release of PAF (apical+basolateral). Maximal stimulation in both apical and total release of PAF occurred at 1.0 ppm O3 (405 +/- 47 and 282 +/- 23% of air control values, respectively, n = 7). The 1.0 ppm O3-induced increased PAF release was significantly inhibitable by the PLA2 inhibitor mepacrine (1 mM), suggesting a connection between PAF release and PLA2 activation. O3 exposure activated PLC in GPTE cells in a concentration- (0.1-1.0 ppm) and time-dependent (10-60 min) manner to produce a significant accumulation of inositol-1,4,5-triphosphate, with maximal accumulation at 1.0 ppm O3 for 1 hr (417 +/- 121% of air control, n = 6). PAF receptor antagonists Ro 24-4736 (1 microM) and Ro 41-5036 (1 microM) did not affect O3-stimulated inositol phosphate accumulation. PLD also was activated in GPTE cells exposed to 1.0 ppm O3 for 1 hr (169 +/- 80% of air control, n = 5). These results suggest that GPTE cells respond to O3 exposure in vitro by increasing production and/or release of PAF via a mechanism that may involve activation of PLA2, PLC, and PLD. Epithelial-derived mediators, such as PAF, may play a role in the pathogenesis of lesions associated with inhalation of O3.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0041-008X
pubmed:author
pubmed:issnType
Print
pubmed:volume
127
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27-36
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Ozone stimulates release of platelet activating factor and activates phospholipases in guinea pig tracheal epithelial cells in primary culture.
pubmed:affiliation
Department of Toxicology, North Carolina State University, Raleigh 27695.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't