Intracellular adhesion molecule 1 ICAM

Oxidatively modified LDL up-regulates the surfece expression of VCAM-1 and intracellular adhesion molecule-1 (ICAM-1) in cultured endothelial cells, promoting the interactions between both cell types (Kume et al., 1992). This may play a pivotal role in the development of atherosclerosis by promoting the penetration of circulating monocytes into the suben-dothelial space whilst inhibiting the mobility of resident macrophages. It has been previously demonstrated that ICAM-1, E-selectin, and VCAM-1 are up-regulated in the microvasculature of rheumatoid but not control synovium (Corkill et al., 1991 Koch et al., 1991). The association between ox-LDL and increased expression of adhesion molecules in the inflamed synovium has yet to be studied. 

ICAM-1 Intracellular adhesion molecule 1 (ICAM-1), an immunoglobulin, plays an important role in the transport and activation of leukocytes. In Crohn s disease (inflammation of the alimentary tract), there is an overexpression of ICAM-1, which causes inflammation. Laboratory studies show that antisense oligonucleotides can reduce the expression of ICAM-1 and hence inflammation. 

SECs, like the vascular endothehum, play an active part in the control of leucocyte recruitment in cases of acute and chronic inflammatory conditions. Eeucocyte recruitment from the blood compartment is a crucial determinant for the induction of immunity and inflammation. SECs control this process by producing cytokines that activate leucocytes and by expressing adhesion molecules. Under inflammatory conditions upregulation of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was found [35 36], as well as expression of E-selectin and P-selectin [37]. Together with the expression of CD4 on SECs it has been postulated that these adhesion molecules might also be involved in the adhesion of KC cells to the sinusoidal wall [20]. 

The intracellular adhesion molecule-1 (ICAM-1) is an important protein of endothelial cells. Its expression is induced by the proinflammatory cytokines IL-I, TNF-a, and INF-y during the early phase of the inflammatory process. Under these conditions, its soluble form, sICAM-1, is released intrathecally at a high rate, probably originating from the endothelial cells of the inflamed tissue (i.e., the meninges and adjacent brain parenchymal tissue). 

Psoriasis is a disease of the immune system that involves T lymphocytes. The etiology and pathogenesis of psoriasis results from complex communications that cause activation of T lymphocytes and trafficking to the skin. Further reactivation causes inflammation and overproduction of skin, resulting in lesions and plaques. In psoriatic skin, there is an upregulation of intracellular adhesion molecule-1 (ICAM-1) on endothelium and keratinocytes. 

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). 

Alicaforsen - Isis Pharmaceuticals Antisense oligonucleotide Phase 3 Inhibitor of intracellular adhesion molecule-1 (ICAM-1) Crohn s disease... 

In other studies, intrapleural tetracycline was found to cause an acute and rapid rise in the level of interleukin-8, which correlated with the presence of neutrophils in pleural fluids of patients (50). In in vitro studies, we investigated whether talc stimulated pleural mesothelial cells to release C-X-C and/or C-C chemokines. We found that both IL-8 and MCP-1 release were induced in pleural mesothelial cells stimulated by talc (51). This release of chemokines is associated with several other phenomena including the expression of intracellular adhesion molecule-1 (ICAM-1). ICAM-1 is an adhesion molecule that binds with its natural ligand (CDl 1-CD18) receptors on leukocytes, which then transmigrate across the inflamed mesothelium into the pleural space in response to talc. Release of IL-8 and MCP-1 by talc-stimulated mesothelial cells required active phagocytosis of the talc particles by mesothelial cells. Inhibition of phagocytosis inhibited chemokine release. 

The production of inflammatory cytokines and cell adhesion molecules (CAMs) by the arterial endothelium are key cellular events involved in the development of atherosclerosis. Activation of the endothelium results in the release of vascular cytokines such as interleukin-1 (IL-la) and tumor necrosis factor alpha (TNF-a). These cytokines induce the expression of CAMs such as intracellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1), which, together with activated monocyte chemoattractant protein-1 (MCP-1), recruit monocytes through the vascular wall, where they are involved in foam cell formation. The nuclear transcription factor, NF-kB, is a mediator in TNF-a-induced expression of cell adhesion molecules and MCP. NF-kB is activated by an atherogenic diet (Liao et al. 1993) and oxidized LDL (Brand et al. 1997), and activation is inhibited by various antioxidants (Kunsch and Medford 1999). Therefore it is of particular interest that GEN attenuated NF-kB DNA binding and TNF-a release in human monocytes (Shames et al. 1999). A small, uncontrolled pilot study ( = 6) found that GEN, but not DAI, inhibited TNF-a-induced NF-kB activation in ex vivo human lymphocytes following consumption of 100 mg isoflavones/day for 3 weeks, as well as in cultured human... 

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