Linked Life Data

8997258

Source:http://linkedlifedata.com/resource/pubmed/id/8997258

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Pt 1
pubmed:dateCreated
1997-2-12
pubmed:abstractText
Although substance P (SP) has been shown to mediate microvascular leakage in response to various stimuli, some data suggest that, in contrast, SP may play a protective role in the maintenance of airway epithelial integrity. To investigate the effect of SP on epithelial barrier function, we measured paracellular mannitol flux and the transepithelial potential difference (PD) of human bronchial epithelial (HBE) and canine bronchial epithelial (CBE) cells. Incubation of confluent cell cultures with SP had no effect on baseline flux. However, pretreatment inhibited the flux-enhancing effects of 0.5 ppm ozone by 50% in HBE cells and 40% in CBE cells and inhibited the ozone-induced decrease in PD in CBE cells by 54%. SP-afforded protection was reduced by the neurokinin (NK)-1 receptor antagonist CP-96,345.NK1 and NK3 receptor agonists also inhibited ozone-induced permeability, whereas an NK2 receptor agonist was without significant effect. These data indicate that SP exerts a protective effect on bronchial epithelial barrier function under conditions of challenge, which appears to be mediated in large part through NK1 receptors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L889-95
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Protective effect of substance P on permeability of airway epithelial cells in culture.
pubmed:affiliation
Department of Environmental Health Sciences, Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.