Open AccessIntercellular adhesion molecule‐1 (ICAM‐1) expression and soluble ICAM‐1 (sICAM‐1) production by cytokine‐activated human aortic endothelial cells: a possible role for ICAM‐1 and sICAM‐1 in atherosclerotic aortic aneurysms
Author(s) -
SZEKANECZ Z.,
SHAH M. R.,
PEARCE W. H.,
KOCH A. E.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06147.x
Subject(s) - icam 1 , intercellular adhesion molecule 1 , cytokine , cell adhesion molecule , inflammation , immunology , tumor necrosis factor alpha , endothelium , vcam 1 , cell adhesion , endothelial stem cell , endothelial activation , intercellular adhesion molecule , biology , proinflammatory cytokine , microbiology and biotechnology , medicine , in vitro , cell , endocrinology , biochemistry
SUMMARY The interactions of inflammatory cells, cytokines, and cell adhesion molecules (CAM) may be important in the pathogenesis of vascular diseases such as abdominal aortic aneurysms (AAA), in which inflammation plays a role. The aim of this study was to investigate the pathogenic role of ICAM‐1, a molecule involved in leucocyte‐endothelial interactions, in vascular inflammation. ELISA of human explant culture supernatants revealed a four‐fold increase in sICAM‐1 production by AAA (n = 9) versus normal (n = 8) aortic explants. Human aortic endothelial cell (hAEC) culture was used for further studies as an in vitro model for aortic inflammatory conditions. Tumour necrosis factor‐alpha (TNF‐α) or IL‐β treatment of hAEC resulted in an up to 1‐8‐fold significant increase in sICAM‐1 production compared with resting cells. In addition, the expression of ICAM‐1 on cytokine‐stimulated versus resting hAEC was measured by radioimmunoassay. TNF‐α significantly induced ICAM‐1 expression on these cells. These results suggest that different forms of ICAM‐1, present on or released by the activated aortic endothelium, may be involved in leucocyte adhesion to and migration into the vessel wall.