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dc.contributor.author Scott, DA
dc.contributor.author Palmer, RM
dc.date.accessioned 2016-01-13T22:03:38Z
dc.date.available 2016-01-13T22:03:38Z
dc.date.issued 2003-01-15
dc.identifier.citation Tobacco Induced Diseases. 2003 Jan 15;1(1):7
dc.identifier.uri http://dx.doi.org/10.1186/1617-9625-1-1-7
dc.identifier.uri http://hdl.handle.net/1993/31055
dc.description.abstract Abstract Sequential interactions between several adhesion molecules and their ligands regulate lymphocyte circulation and leukocyte recruitment to inflammatory foci. Adhesion molecules are, therefore, central and critical components of the immune and inflammatory system. We review the evidence that tobacco smoking dysregulates specific components of the adhesion cascade, which may be a common factor in several smoking-induced diseases. Smoking causes inappropriate leukocyte activation, leukocyte-endothelial adhesion, and neutrophil entrapment in the microvasculature, which may help initiate local tissue destruction. Appropriate inflammatory reactions may thus be compromised. In addition to smoke-induced alterations to membrane bound endothelial and leukocyte adhesion molecule expression, which may help explain the above phenomena, smoking has a profound influence on circulating adhesion molecule profiles, most notably sICAM-1 and specific sCD44 variants. Elevated concentrations of soluble adhesion molecules may simply reflect ongoing inflammatory processes. However, increasing evidence suggests that specific soluble adhesion molecules are immunomodulatory, and that alterations to soluble adhesion molecule profiles may represent a significant risk factor for several diverse diseases. This evidence is discussed herein.
dc.title The influence of tobacco smoking on adhesion molecule profiles
dc.type Journal Article
dc.language.rfc3066 en
dc.rights.holder Scott and Palmer.
dc.date.updated 2016-01-12T14:15:08Z


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