Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-7-30
pubmed:abstractText
Recruitment of neutrophils into the alveoli plays a major role in the pathogenesis of acid-induced pneumonitis. Preliminary data suggest that alteration in the expression of cellular adhesion molecules on the airway epithelial cells may play an important role in the recruitment of neutrophils following acid-induced lung injury. The aim of this study was to evaluate the change in the surface expression of intercellular adhesion molecule-1 (ICAM-1), E-cadherin, and vascular cell adhesion molecule -1 (VCAM-1) on acid-exposed A549 alveolar lining epithelial cells by flow cytometry and confocal laser microscopy. Acid exposure changed cell morphology, increased cell adhesion after trypsin-EDTA treatment, and up-regulated the expression of ICAM-1 and E-cadherin but not of VCAM-1. The up-regulation of ICAM-1 expression will induce the dysfunction of epithelial cells with or without accumulation of neutrophils in air spaces. Because the distribution of E-cadherin in acid-exposed A549 cells was at the sites where the cells attached to culture dish but not at the intercellular junctions between adjoining cells, up-regulated expression of E-cadherin will rather result in alterations of epithelial morphology and function of epithelial barrier. In addition, pentoxifylline suppressed the up-regulation of ICAM-1 and E-cadherin expression and may therefore attenuated the airway inflammation in acid-induced pneumonitis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0190-2148
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
389-400
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Acid exposure potentiates intercellular adhesion molecule-1 and e-cadherin expression on A549 alveolar lining epithelial cells.
pubmed:affiliation
Department of Respiratory Medicine, Juntendo University School of Medicine Tokyo, Japan. aohwada@juntendo.gmc.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't