ICAM-1 expression

Wang GJ, Deng HY, Maier CM, Sun GH, Yenari MA. Mild hypothermia reduces ICAM-1 expression, neutrophil infiltration and microglia/monocyte accumulation following experimental stroke. Neuroscience 2002 114 1081-1090. 

Gentile, C. et al.. Antioxidant betalains from cactus pear (Opuntia ficus- indica) fruit inhibit endothelial ICAM-1 expression, Ann. NY Acad. ScL, 1028, 481, 2004. 

Albanesi, C., Cavani, A., and Girolomoni, G., IL-17 is produced by nickel-specific T lymphocytes and regulates ICAM-1 expression and chemokine production in human keratinocytes synergistic or antagonistic effects with IFN-y and TNF-a. J. Immunol. 162, 494-502, 1999. 

Madjdpour C, Oertli B, Ziegler U, Bonvini JM, Pasch T, Beck-Schimmer B (2000) Lipopolysaccharide induces functional ICAM-1 expression in rat alveolar epithelial cells in vitro. Am J Physiol 278(3) L572-L579... 

Paine R 3rd, Christensen P, Toews GB, Simon RH (1994) Regulation of alveolar epithelial cell ICAM-1 expression by cell shape and cell-cell interactions. Am J Physiol 266(4 Pt 1) L476-L484... 

Paolieri F, Battifora M, Riccio AM Terfenadine and fexofenadine reduce in vitro ICAM-1 expression on human continuous cell lines. Ann Allergy Asthma Immunol 1988 81 601-607. 

Tang A. Udey MC Doses of ultraviolet radiation that modulate accessory cell activity and ICAM-1 expression are ultimately cytotoxic for murine epidermal Langerhans cells. J Invest Dermatol 1992 99 71S-73S. 

Cheng et al. showed that intravenous infusion of intracellular adhesion molecule (ICAM) AS-ODN markedly reduced ICAM-1 expression, alleviated infiltration of inflammatory cells and accumulation of extracellular matrix in the obstructed kidney of mice with unilateral obstruction of the ureter [133],... 

Kobuchi, H., Roy, S., Sen, C.K., Nguyen, H.G., and Packer, L., Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway. Am. J. Physiol, 277, C403, 1999. 

Recent evidence suggests that atherosclerosis is a chronic inflammatory process. The recruitment of mononuclear leukocytes and formation of intimal macrophage-rich lesions at specific sites of the arterial tree are key events in atherogenesis. Alterations of chemotactic and adhesive properties of the endothelium play an important role in this process [82]. Quercetin has been reported to inhibit the expression in glomerular cells of monocyte chemoattractant protein-1 (MCP-1) [83] a potent chemoattractant for circulating monocytes. Red wine reduced MCP-1 mRNA and protein expression in abdominal aorta of cholesterol fed rabbits after balloon injury and this effect was associated with a reduced neointimal hyperplasia [84]. The antioxidant-mediated inhibition of nuclear factor k B (NFkB) and the subsequent non selective reduction of cytokine transcription have been suggested to be responsible for these effects [83]. Additionally, quercetin downregulated both phorbol 12-myristate 13-acetate (PMA)- and tumour necrosis factor-a (TNFa)-induced intercellular adhesion molecule-1 (ICAM-1) expression in human endothelial cells [86]. 

IL-1 IL-2, TNF, GM-CSF, Ag presentation Fever, acute-phase protein response, hypotension, increased ICAM-1 expression (endothelial cells) IL-2, IL-4, IL-6, TNF, PGE2, collagenase Macrophages, endothelial cells... 

We speculate that ischemia induces changes in the tubulo-interstitium by such factors as oxidative stress, apoptosis, an increase in intracellular Ca, complement activation, ICAM-1 expression, and inflammation, in a region controlled by the blood vessels, thereby influencing the blood vessels and prolonging vascular spasm. Coronary spasm persists for 15min, and cerebrovascular spasm in the presence of subarachnoid hemorrhage persists for a week in some patients. Therefore, renovascular spasm may persist for a long period. 

Inhibits high dose glucose-induced ICAM-1 expression via AMP-activated protein kinase and PPAR-gamma activations in endothelial cells [ 130]... 

Wang et al., 2002 SD rats MCAo 2 h, with 33 and 37, intraischemia reperfusion Infarct size, ICAM-1 expression, neutrophil and monocyte infiltration, microglial activation at 1 d, 3 d, and 7 d postischemia Reduced infarct size, ICAM-1, neutrophils and monocytes, and microglial activation... 

Cellular responses, as measured by a mixed-lymphocyte reaction, cytotoxic T lymphocyte response, and NK cell activity, were all undiminished, and if anything, there was a slight increase in CTL and NK responses. As would be expected by the histologic profile and the known increases in cytokine and chemokine production associated with the administration of PS ODNs in rodents, in this series of experiments there was no diminution in immune response. Administering a mouse-specific ICAM-1 inhibitor produced reductions in mixed lymphocyte reactions. This inhibition was expected as this is one of the desired pharmacologic effects of reducing ICAM-1 expression. 

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]. 

It was proved that at non-toxic doses, PPD induces intercellular adhesion molecule-1 (ICAM-1) expression on the keratinocytes [16]. These results were consistent with the view that oxidative stress may be an essential part of the pre-immunological phase in the induction of the allergic contact dermatitis by PPD [16]. 

Picardo M, Zompella C, Marchese C, De-Luca C, Faggioni A, Schmidt RJ, Santucci B. Paraphenyiene diamine a control allergen, induces oxidative stress and ICAM-1 expression in human keratinocytes. Brit J Dermatol 1992 126 450-455. 

Czech, W., Krutmann, J., Budnik, A., Schopf, E. and Kapp, A. (1993). Induction of intercellular adhesion molecule 1 (ICAM-1) expression in normal human eosinophils by inflammatory cytokines. J. Invest. Dermatol. 100, 417-423. 

It seems likely that MBP exerts some efiects on epithelial function at much lower concentrations than those required to produce cellular dysfunction and detachment. Over a 24 h exposure period human nasal epithelium showed a 50% u[)-regulation of intercellular adhesion molecule-1 (ICAM-1) expression when exposed to concentrations of MBP within the range 0.1—0.2 ftgmP (Ayars et al., 1991). 

Ayars, G.H., Altman, L.C, Loegering, D.A. and Gleich, G.J. (1991). Eosinophil major basic protein [MBP] up regulates intercellular adhesion molecular-1 [ICAM-1] expression on human nasal epithelial cells [HNE]. J. Allergy Clin. Inununol. 87, 304. 

Various studies have also examined animal models of pulmonary inflammation that are representative of primary eosinophil or neutrophil infiltration. Lung inflammation characterized by eosinophil influx has been used as a model of asthma and is not generally associated with lung fibrosis. After several episodes of repeated antigen challange, a subset of Ascaris -sensitive Cynomolgus monkeys developed a persistent eosinophilia and enhanced intercellular adhesion molecule-1 (ICAM-1) expression on pulmonary endothelial and epithelial cells when compared to control animals (Gundel etal., 1991, 1992). 

Weiss JM, PHarski KA> Weyl A, et al. Prostaglandin El inhibits TNF a-induced T-ceU adhesion to endothelial cells by selective down-modulation of ICAM-1 expression on endothelial cells. Exp Dermatol 1995 4 302-7. 

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