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Article: Circulating adhesion molecules in asthma

TitleCirculating adhesion molecules in asthma
Authors
Issue Date1994
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
American Journal Of Respiratory And Critical Care Medicine, 1994, v. 149 n. 5, p. 1149-1152 How to Cite?
AbstractThere is increasing evidence that leukocyte-endothelial adhesion molecules are important in inflammatory airway disease because of their involvement in the primary steps of entrapment and migration of leukocytes to the site of inflammation. Recently, circulating forms of these adhesion molecules have been described, although their origin, fate, and function are still unknown. We have used an antigen capture ELISA to measure the concentrations of circulating intercellular adhesion molecule-1 (cICAM-1), E-selectin (cE- selectin), and vascular cell adhesion molecule-1 (cVCAM-1) in the peripheral blood of 13 atopic and 16 nonatopic normal subjects, 29 patients with stable asthma, and inpatients with acute asthma on Day 1 (n = 38), Day 3 (n = 29), and Day 28 (n = 13) of an asthmatic episode. Circulating ICAM-1 and E- selectin levels were significantly raised in acute asthma on all three study days when compared with those observed in stable asthma, atopic normal, or nonatopic normal volunteers with no significant differences among the latter three groups. Circulating VCAM-1 was not significantly increased in any of the groups studied. There were no correlations among the concentrations of these three circulating adhesion molecules. The elevated concentrations of cICAM-1 and cE-selectin in acute asthma may reflect the extensive inflammatory response occurring in the airways during acute exacerbations of the disease with airway obstruction. It is possible that the cytokine and mediator profiles in acute asthma lead to the preferential synthesis and expression of these two circulating adhesion molecules in comparison with cVCAM-1.
Persistent Identifierhttp://hdl.handle.net/10722/162047
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMontefort, Sen_HK
dc.contributor.authorLai, CKWen_HK
dc.contributor.authorKapahi, Pen_HK
dc.contributor.authorLeung, Jen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorChan, HSen_HK
dc.contributor.authorHaskard, DOen_HK
dc.contributor.authorHowarth, PHen_HK
dc.contributor.authorHolgate, STen_HK
dc.date.accessioned2012-09-05T05:16:53Z-
dc.date.available2012-09-05T05:16:53Z-
dc.date.issued1994en_HK
dc.identifier.citationAmerican Journal Of Respiratory And Critical Care Medicine, 1994, v. 149 n. 5, p. 1149-1152en_HK
dc.identifier.issn1073-449Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/162047-
dc.description.abstractThere is increasing evidence that leukocyte-endothelial adhesion molecules are important in inflammatory airway disease because of their involvement in the primary steps of entrapment and migration of leukocytes to the site of inflammation. Recently, circulating forms of these adhesion molecules have been described, although their origin, fate, and function are still unknown. We have used an antigen capture ELISA to measure the concentrations of circulating intercellular adhesion molecule-1 (cICAM-1), E-selectin (cE- selectin), and vascular cell adhesion molecule-1 (cVCAM-1) in the peripheral blood of 13 atopic and 16 nonatopic normal subjects, 29 patients with stable asthma, and inpatients with acute asthma on Day 1 (n = 38), Day 3 (n = 29), and Day 28 (n = 13) of an asthmatic episode. Circulating ICAM-1 and E- selectin levels were significantly raised in acute asthma on all three study days when compared with those observed in stable asthma, atopic normal, or nonatopic normal volunteers with no significant differences among the latter three groups. Circulating VCAM-1 was not significantly increased in any of the groups studied. There were no correlations among the concentrations of these three circulating adhesion molecules. The elevated concentrations of cICAM-1 and cE-selectin in acute asthma may reflect the extensive inflammatory response occurring in the airways during acute exacerbations of the disease with airway obstruction. It is possible that the cytokine and mediator profiles in acute asthma lead to the preferential synthesis and expression of these two circulating adhesion molecules in comparison with cVCAM-1.en_HK
dc.languageengen_US
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.orgen_HK
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicineen_HK
dc.subject.meshAcute Diseaseen_US
dc.subject.meshAdulten_US
dc.subject.meshAsthma - Blooden_US
dc.subject.meshCell Adhesion Molecules - Blooden_US
dc.subject.meshE-Selectinen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshIntercellular Adhesion Molecule-1en_US
dc.subject.meshMaleen_US
dc.subject.meshVascular Cell Adhesion Molecule-1en_US
dc.titleCirculating adhesion molecules in asthmaen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, J: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, J=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1164/ajrccm.149.5.7513593-
dc.identifier.pmid7513593-
dc.identifier.scopuseid_2-s2.0-0028266361en_HK
dc.identifier.volume149en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1149en_HK
dc.identifier.epage1152en_HK
dc.identifier.isiWOS:A1994NP83900014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMontefort, S=6701353725en_HK
dc.identifier.scopusauthoridLai, CKW=7403086390en_HK
dc.identifier.scopusauthoridKapahi, P=18734499500en_HK
dc.identifier.scopusauthoridLeung, J=7202180349en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridChan, HS=26024631700en_HK
dc.identifier.scopusauthoridHaskard, DO=7102594554en_HK
dc.identifier.scopusauthoridHowarth, PH=7103350375en_HK
dc.identifier.scopusauthoridHolgate, ST=7201795361en_HK

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