Endothelial leukocyte adhesion expression

B. N. Cronstein, S. C. Kimmel, R. I. Levin, F. Martiniuk, and G. Weissmann, A mechanism for the antiinflammatory effects of corticosteroids the glucocorticoid receptor regulates leukocyte adhesion to endothelial cells and expression of endothelial-leukocyte adhesion molecule 1 and intercellular adhesion molecule 1, Proc. Natl. Acad. Sci. USA 89 9991-9995 (1992). 

Upregulation of adhesion molecules has been documented in human stroke patients [7]. It was demonstrated that leukocytes from patients suffering an ischemic stroke or transient ischemic attack showed increased CDl la expression within 72 hours of the onset of symptoms [123]. Increased ICAM-1 expression on the surface of vessels fi om cerebral cortical infarcts was detected in four patients [124]. In some studies, soluble isoforms of adhesion molecules shed fi om the surfaces of activated cells were quantified in serum. Serum endothelial-leukocyte adhesion molecule-1 (ELAM-1, E-selectin) levels increased up to 24 hours after stroke. Similar increases were observed in serum vascular cell adhesion molecule-1 (VCAM-1) levels and these increases were sustained up to 5 days [125]. In contrast, serum ICAM-1 levels in acute ischemic stroke patients have been found to be lower than or the same as those of asymptomatic control subjects matched for age, sex, and vascular risk factors [125,126]. The reason not to detect an increase in serum levels of adhesion molecules might be due to the late enrolling of patients. Once adhesion molecules bind to leukocytes and endothelial cells, they can no longer be detected in serum [7]. 

X. Wang, T. L. Yue, F. C. Barone, and G. Z. Feuerstein, Demonstration of Increased Endothelial-Leukocyte Adhesion Molecule-1 mRNA Expression in Rat Ischemic Cortex, Stroke. 26 (1995) 1665-1669. 

Kyan-Aung, U., Haskard, D.O., Poston, R.N., Thornhill, M.H. and Lee, T.H. (1991). Endothelial leukocyte adhesion molecule 1 and intercellular adhesion molecule 1 mediate adhesion of eosinophils to endothelial cells in vitro and are expressed by endothelium in allergic cutaneous inflammation in vitro. J. Immunol. 146, 521-528. 

Leung, D.Y., Pober, J.S. and Cotran, KS. (1991). Expression of endothelial-leukocyte adhesion molecule-1 in elicited late phase allergic reactions. J. Clin. Invest. 87, 1805-1809. 

Montefort, S., Roche, W.R, Howarth, P.H., Djukanovic, R, Gratziou, C., Carroll, M., Smith, L., Britten, K.M., Haskard, D., Lee, T.H. and Holgate, S.T. (1992). Intercellular adhesion molecule-1 (ICAM-1) and endothelial leukocyte adhesion molecule-1 (ELAM-1) expression in the bronchial mucosa of normal and asthmatic subjects. Eur. Respir. J. 5, 815-823. 

The innervation of the lymphoid vasculature by substance P-containing neurons and the ability of substance P to enhance lymph tissue blood flow (Lundbeig et al., 1985) suggest that substance P may alter lymphocyte traffic . Substance P induces the expression of endothelial leukocyte adhesion molecule 1 (ELAM-1) on microvascular endothelial cells (Matis et al., 1990) and may similarly affect the expression of adhesion molecules on lymphocytes. Infusion of substance P has been shown to increase lymph flow and lymphocyte traffic in sheep lymph nodes (Moore etal., 1989). 

Matis, W.L., Lavker, R.M. and Murphy, G.F. (1990). Substance P induces the expression of an endothelial-leukocyte adhesion molecule by microvascular endothelium. J. Invest. Dermatol. 94, 492-495. 

Wang, X., Yue, T.-L., Barone, F. C., and Feuerstein, G. Z., Demonstration of increased endothelial-leukocyte adhesion molecule-1 mRNA expression in rat ischaemic cortex, Stroke, 26, 1665, 1995. 

Increased cytokine production may also play a role in silica-induced autoimmune vascular disease. Adhesion molecule expression is elevated on vascular endothelial cells in response to TNF-a and IL-1. Adhesion molecules such as endothelial leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) recruit inflammatory cells to specific sites on the vascular endothelium, and it has been hypothesized that vascular pathology following silica exposure may be the result of this interaction (Nowack et al., 1998). IFN-y is expressed at elevated levels by lymphocytes in silicotic thoracic lymph nodes and may be responsible for the long-lasting inducible nitric oxide synthase (iNOS) expression in these tissues (Friedetzky et al., 2002). The increase in IFN-y may also cause a shift towards a dominant Thl response, contributing to the maintenance of a chronic inflammatory state in silica-containing lymph nodes (Gam et al., 2000). 

Hession, C., Osborn, L, Goff, D., Chi-Rosso, G., Vassallo, C., Pasek, M., Pittack, C., Tizard, R., Goelz, S., McCarthy, K., Hopple, S., and Lobb, R., 1990, Endothelial leukocyte adhesion molecule 1 Direct expression cloning and functional interactions, Proc. Natl. Acad. Sci. USA 87 1673-1677. 

Murase, T., Kume, N., Hase, T., Shibuya, Y., Nishizawa, Y., Tokimitsu, I., and Kita, T., Gallates inhibit cytokine-induced nuclear translocation of NF-kappaB and expression of leukocyte adhesion molecules in vascular endothelial cells, Arterioscler. Thromb. Vase. Biol, 19, 1412, 1999. 

Cybulsky, M. I. and Gimbrone, M. A., Jr. (1991). Endothelial expression of mononuclear leukocyte adhesion molecule during atherogenesis. Science 251,788-791. 

Oxidised LDL in the artery wall initiates a series of reactions designed to repair the damage it causes. Initial damage triggers an inflammatory response. Monocytes enter the artery waU from the bloodstream, with platelets adhering to the area of insult. This may be promoted by induction of factors such as vascular ceU adhesion molecule 1 (VCAM-1), a cell-surface sialoglycoprotein that is expressed by cytokine-activated endothelium. This membrane protein mediates leukocyte-endothelial cell adhesion and signal transduction, and may play a role in the development of atherosclerosis and rheumatoid arthritis. 

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