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Tobacco Induced Diseases

, 1:7

First Online: 15 January 2003Received: 18 December 2001Revised: 18 February 2002Accepted: 19 February 2002DOI: 10.1186-1617-9625-1-1-7

Cite this article as: Scott, D. & Palmer, R. Tob. Induced Dis. 2003 1: 7. doi:10.1186-1617-9625-1-1-7


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.

Abbreviations usedCIPDchronic inflammatory periodontal disease

COPDchronic obstructive pulmonary disease

GCFgingival crevicular fluid

HUVEChuman umbilical vein endothelial cells

ICAM-1intercellular adhesion molecule-1 CD54

LFA-1lymphocyte functional antigen-1 CD11a-CD18; αLβ2

Mac-1CD11b-CD18 αMβ2

PECAM-1platelet-endothelial cell adhesion molecule-1

VCAM-1vascular cell adhesion molecule-1 CD106.

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Autor: DA Scott - RM Palmer


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