Endothelial leucocyte adhesion

ELAM-1 Endothelial leucocyte adhesion molecule-1 ELF Respiratory epithelium lung fluid... 

EPA Eicosapentaenoic acid EpDIF Epithelial-derived inhibitory factor also known as epithelium/derived relaxant fector EPO Eosinophil peroxidase EPOR Erythropoietin receptor EPR Effector cell protease EPX Eosinophil protein X ER Endoplasmic reticulum ERCP Endoscopic retrograde cholangiopancreatography E-selectin Endothelial selectin formerly known as endothelial leucocyte adhesion molecule-1 (ELAM-1)... 

I and endothelial leucocyte adhesion molecule 1 or E-selectine, and expression of MHC class... 

I. M. Cybulsky and M. A. Gimbione Jr, Endothelial-leucocyte adhesion molecules in acute inflammation and atherogenesis. In Endothelial Cell Dysfunction... 

Bevilacqua, M. R, Endothelial-leucocyte adhesion molecules, Annu. Rev. Immunol., 11, 767, 1993. 

Graber, N., Gopal, T. V., Wilson, D., Beall, L. D., Polte, T., and Newman, W., T cells bind to cytokine-activated endothelial cells via a novel, inducible sialoglycoprotein and endothelial leucocyte adhesion molecule-1, J. Immunol., 145, 819, 1990. 

BENTLEY, A.M., DURHAM, S.R., ROBINSON, D.R., HAMID, Q KAY, A.B. DURHAM, S.R. (1992) Expression of the endothelial leucocyte adhesion molecules ICAM-1, E-selectin and UCAM-1 in the bronchial mucosa in steady state asthma and allergen-induced asthma. Thorax, 47, 852P (Abstract). 

Cronstein B, Kimmel 8, Lenin R, Martiniuk F, Weissmann G. A mechanism for the anti-inflammatory effects of corticosteroids the glucocorticoid receptor regulates leucocyte adhesion to endothelial cells and expression of endothelial-leucocyte adhesion molecule-1 and intercellular adhesion molecule-1. Proc Natl Acad Sci U8A 1992 89 9991-9995. 

Kume, N., Cybulsky, M.I. and Gimbrone, M.A. (1992). Lysophosphatidylcholine, a component of atherogenic lipoproteins, mediates mononuclear leucocyte adhesion in cultured human and rabbit endothelial cells. J. Clin. Invest. 90, 1138-1144. 

Inhibition of leucocyte adhesion to endothelium. By acting on the gene transcription factor called nuclear factor kappa B (NFkB), NO limits the expression by endothelial cells of monocyte chemotactic protein-1 (MCP-1) and VCAM-1. As both MCP-1 and VCAM-1 are involved with pro-inflammatory responses, NO is in this manner an anti-inflammatory agent ... 

Effect on ROS-mediated events Leucocyte adhesion to endothelial cells provoked by oxLDL FO Hamster Reference (38)... 

Hyperforin, a component of Hypericum perforatum L. (Saint John s-wort) incubated with human coronary endothelial cells reduced the expression of endothehal leucocyte adhesion molecules ICAM-1 (interceUular ceU adhesion molecule-1, CD54) and VCAM-1 (vascular cell adhesion molecule-1, CD 196), whereas the expression of E-selectin... 

Both nonselective (h/°-monomethyl-L-arginine) and specific (W-iminomethyl-L-lysine) inhibitors of iNOS significantly increased leucocyte binding by normal human intestinal microvascular endothelial cells activated with cytokines and Hpopolysaccha-ride, but had no effect on leucocyte adhesion by similarly activated inflammatory bowel disease human intestinal microvascular endothelial cells (Bi-NiON et al. 2000). 

Studies have shown that niacin significantly reduces ICAM-1, VCAM-1, PECAM and E-selectin levels. It also reduced the tumour necrosis (actor-alpha (TNF-a) induced rise in ICAM (it does this by reducing mRNA-induced expression of ICAM). It also decreased the production of ICAM through its reduction in interferon-y (IFN-y) and interleukin-1 (IL-l). Through these mechanisms, niacin induces a reduction of monocyte adhesion in endothelial cells This may possibly lead to decreased leucocyte adhesion to endothelium, which is an important early event in atherosclerosis (Tavintharan et al. 2009). 

The recruitment and migration of leucocytes into inflamed tissues is a carefully orchestrated process (Figure 7.1). It consists of sequential steps mediated by different families of adhesion molecules expressed by both the leucocytes and the endothelial cells at the site of inflammation [4]. Of these adhesion molecules, the selectin family mediates the initial contact and subsequent rolling of the leucocyte on the endothelium. It consists of three members, i.e. E- (endothelial), P- (platelet) and L- (leucocyte) selectin. Activated endothelial cells express E- and P-selectin. P-selectm is also expressed on platelets, whereas L-selectin is only expressed on subsets of leucocytes [5]. 

In most, if not all, chronic inflammatory diseases endothelial cells are prominently involved in the disease process. This is demonstrated by an increased expression of adhesion molecules and production of cytokines, and their pro-angiogenic behaviour. This leads to continuous recruitment of leucocytes into the inflamed area, without (detectable) antigen present in the affected tissue, resulting in a vicious circle of tissue damage and leucocyte recruitment. Targeting inhibitory agents (in)to the endothelial cell may interrupt in this process by controlling the activation status of this cell type. 

After infection and immune cell activation, endothelial cells are variously activated to bind peripheral blood leucocytes. Bacterial toxins such as lipopolysaccharide (LPS), inflammatory cytokines such as tumour necrosis factors a and (5 (TNFa and TNFP) and interleukin-1 (5 (IL-ip) increase the synthesis of cell surface E- and P-selectins in endothelial cells. Histamine and thrombin increase PM P-selectins in endothelial cells and platelets. L-selectins are constitutively expressed in monocytes and lymphocytes. The selectins are involved in the initial adhesion of leucocytes with endothelial cells via selectin-selectin receptor interactions, for example, monocyte L-selectin-endothelial L-selectin ligand binding and T-lymphocyte-endothelial selectin-integrin interactions. This initial phase of leucocyte-endothelial adhesion enables an early stage of leucocyte rolling through successive formation and breakage of adhesive interactions. 

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