Comparative effect of C3a and C5a on adhesion molecule expression on neutrophils and endothelial cells
Identifieur interne : 000695 ( Main/Exploration ); précédent : 000694; suivant : 000696Comparative effect of C3a and C5a on adhesion molecule expression on neutrophils and endothelial cells
Auteurs : E. Foreman [États-Unis] ; M. Glovsky [États-Unis] ; L. Warner [États-Unis] ; J. Horvath [États-Unis] ; A. Ward [États-Unis]Source :
- Inflammation [ 0360-3997 ] ; 1996-02-01.
Abstract
Abstract: Complement activation is known to enhance neutrophil binding to human umbilical vein endothelial cells (HUVECs). Recently, we have shown that recombinant human C5a upregulates P-selectin in HUVECs. Unstimulated human neutrophil binding is also increased on C5a stimulated HUVECs. We demonstrate in this report that C5a upregulates CD11b/CD18 in human neutrophils. Also shown is that synthetic C3a57–77 and an analog 15 amino acid C3a peptide (C3a15) neither upregulate CD11b/CD18 nor do the C3a peptides increase P-selectin, ICAM-1 or E-selectin in HUVECs. Thus C5a and not C3a is responsible for early (∼30 minutes) neutrophil adhesion to endothelial cells after complement activation.
Url:
DOI: 10.1007/BF01487740
Affiliations:
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Ward</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4DD89A8B6FB55BB0C6765CF82EA7227689D7E223</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1007/BF01487740</idno><idno type="url">https://api.istex.fr/document/4DD89A8B6FB55BB0C6765CF82EA7227689D7E223/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000644</idno><idno type="wicri:Area/Main/Curation">000644</idno><idno type="wicri:Area/Main/Exploration">000695</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Exploration">000695</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Comparative effect of C3a and C5a on adhesion molecule expression on neutrophils and endothelial cells</title><author><name sortKey="Foreman, E" sort="Foreman, E" uniqKey="Foreman E" first="E." last="Foreman">E. 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Recently, we have shown that recombinant human C5a upregulates P-selectin in HUVECs. Unstimulated human neutrophil binding is also increased on C5a stimulated HUVECs. We demonstrate in this report that C5a upregulates CD11b/CD18 in human neutrophils. Also shown is that synthetic C3a57–77 and an analog 15 amino acid C3a peptide (C3a15) neither upregulate CD11b/CD18 nor do the C3a peptides increase P-selectin, ICAM-1 or E-selectin in HUVECs. Thus C5a and not C3a is responsible for early (∼30 minutes) neutrophil adhesion to endothelial cells after complement activation.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Michigan</li></region></list><tree><country name="États-Unis"><region name="Michigan"><name sortKey="Foreman, E" sort="Foreman, E" uniqKey="Foreman E" first="E." last="Foreman">E. Foreman</name></region><name sortKey="Foreman, E" sort="Foreman, E" uniqKey="Foreman E" first="E." last="Foreman">E. 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