Effect of Linomide on adhesion molecules, TNF-α, nitrogen oxide, and cell adhesion

2005 ◽  
Vol 5 (2) ◽  
pp. 231-239 ◽  
Author(s):  
A. Abdul-Hai ◽  
R. Hershkoviz ◽  
L. Weiss ◽  
O. Lider ◽  
S. Slavin
Keyword(s):  
Cell Adhesion ◽  
Nitrogen Oxide ◽  
Adhesion Molecules ◽  
Tnf Α

TNF-α-induced endothelial cell adhesion molecule expression is cytochrome P-450 monooxygenase dependent

2003 ◽  
Vol 284 (2) ◽  
pp. C422-C428 ◽  
Author(s):  
Makoto Sasaki ◽  
D. Ostanin ◽  
J. W. Elrod ◽  
T. Oshima ◽  
P. Jordan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Nadph Oxidase ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Tnf Α ◽  
Oxidase Inhibition ◽  
Endothelial Adhesion Molecules ◽  
Cytochrome P 450

It is strongly suspected that cytokine-induced gene expression in inflammation is oxidant mediated; however, the intracellular sources of signaling oxidants remain controversial. In inflammatory bowel disease (IBD) proinflammatory cytokines, such as TNF-α, trigger gene expression of endothelial adhesion molecules including mucosal addressin cell adhesion molecule-1 (MAdCAM-1). MAdCAM-1 plays an essential role in gut inflammation by governing the infiltration of leukocytes into the intestine. Several groups suggest that endothelial-derived reduced NADP (NADPH) oxidase produces signaling oxidants that control the expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1). In addition to NADPH oxidase, cytochrome P-450 (CYP450) monooxygenases have also been shown to trigger cytokine responses. We found that in high endothelial venular cells (SVEC4-10), multiple inhibitors of CYP450 monooxygenases (SKF-525a, ketoconazole, troleandomycin, itraconazole) attenuated TNF-α induction of MAdCAM-1, whereas NADPH oxidase inhibition (PR-39) did not. Conversely, E-selectin, ICAM-1, and VCAM-1 induction requires both NADPH oxidase and CYP450-derived oxidants. We show here that MAdCAM-1 induction may depend exclusively on CYP450-derived oxidants, suggesting that CYP450 blockers might represent a possible novel therapeutic treatment for human IBD.

Antibody titers to oxidized LDL are related to serum levels of cell-adhesion molecules, TNF-α and CRP (air-study)

2001 ◽  
Vol 2 (2) ◽  
pp. 78
Author(s):  
J. Hulthe ◽  
J. Wikstrand ◽  
L. Bokemark ◽  
L. Mattsson Hulten ◽  
B. Fagerberg
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Oxidized Ldl ◽  
Serum Levels ◽  
Tnf Α ◽  
Antibody Titers

A chromone analog inhibits TNF-α induced expression of cell adhesion molecules on human endothelial cells via blocking NF-κB activation

2007 ◽  
Vol 15 (8) ◽  
pp. 2952-2962 ◽  
Author(s):  
Sarvesh Kumar ◽  
Brajendra K. Singh ◽  
Anil K. Pandey ◽  
Ajit Kumar ◽  
Sunil K. Sharma ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Human Endothelial Cells ◽  
Induced Expression ◽  
Tnf Α

scholarly journals Lipoxin A4inhibits immune cell binding to salivary epithelium and vascular endothelium

2012 ◽  
Vol 302 (7) ◽  
pp. C968-C978 ◽  
Author(s):  
Sreedevi Chinthamani ◽  
Olutayo Odusanwo ◽  
Nandini Mondal ◽  
Joel Nelson ◽  
Sriram Neelamegham ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Vascular Endothelium ◽  
Cell Adhesion Molecule ◽  
Immune Cell ◽  
Receptor Activation ◽  
Tnf Α ◽  
Cell Adhesion Molecule 1

Lipoxins are formed by leukocytes during cell-cell interactions with epithelial or endothelial cells. Native lipoxin A4(LXA4) binds to the G protein-coupled lipoxin receptors formyl peptide receptor 2 (FPR2)/ALX and CysLT1. Furthermore, LXA4inhibits recruitment of neutrophils, by attenuating chemotaxis, adhesion, and transmigration across vascular endothelial cells. LXA4thus appears to serve as an endogenous “stop signal” for immune cell-mediated tissue injury (Serhan CN; Annu Rev Immunol 25: 101–137, 2007). The role of LXA4has not been addressed in salivary epithelium, and little is known about its effects on vascular endothelium. Here, we determined that interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) receptor activation in vascular endothelium and salivary epithelium upregulated the expression of adhesion molecules that facilitates the binding of immune cells. We hypothesize that the activation of the ALX/FPR2 and/or CysLT1 receptors by LXA4decreases this cytokine-mediated upregulation of cell adhesion molecules that enhance lymphocyte binding to both the vascular endothelium and salivary epithelium. In agreement with this hypothesis, we observed that nanomolar concentrations of LXA4blocked IL-1β- and TNF-α-mediated upregulation of E-selectin and intercellular cell adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cells (HUVECs). Binding of Jurkat cells to stimulated HUVECs was abrogated by LXA4. Furthermore, LXA4preincubation with human submandibular gland cell line (HSG) also blocked TNF-α-mediated upregulation of vascular cell adhesion molecule-1 (VCAM-1) in these cells, and it reduced lymphocyte adhesion. These findings suggest that ALX/FPR2 and/or CysLT1 receptor activation in endothelial and epithelial cells blocks cytokine-induced adhesion molecule expression and consequent binding of lymphocytes, a critical event in the pathogenesis of Sjögren's syndrome (SS).

scholarly journals Endothelial cell adhesion molecule expression in gene-targeted mice

1997 ◽  
Vol 273 (4) ◽  
pp. H1903-H1908 ◽  
Author(s):  
Michael J. Eppihimer ◽  
Janice Russell ◽  
Donald C. Anderson ◽  
Barry A. Wolitzky ◽  
D. Neil Granger
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Wild Type ◽  
Tnf Α ◽  
Endothelial Cell Adhesion Molecules ◽  
Vascular Beds ◽  
Deficient Mice ◽  
Endothelial Cell Adhesion

Gene-targeted mice are now routinely employed as tools for defining the contribution of different leukocyte and endothelial cell adhesion molecules to the leukocyte recruitment and tissue injury associated with acute and chronic inflammation. The objective of this study was to determine whether gene-targeted mice that are deficient in CD11/CD18, intracellular adhesion molecule-1 (ICAM-1), or P-selectin exhibit an altered constitutive or induced expression of the endothelial cell adhesion molecules E- and P-selectin. The gene-targeted mice were all developed in the 129Sv mouse strain and backcrossed into C57Bl/6J mice. The number of backcrosses ranged between 8 (P-selectin) and 10 (CD18 and ICAM-1) generations. The dual-radiolabeled monoclonal antibody technique was used to quantify E- and P-selectin expression in different vascular beds. In the unstimulated state, E-selectin expression was significantly elevated (relative to wild-type mice) in the stomach, large intestine, and brain of mutants deficient in ICAM-1. In general, constitutive expression of P-selectin did not differ between wild-type, ICAM-1-deficient, and CD11/CD18-deficient mutants. In CD11/CD18-deficient mice, tumor necrosis factor-α (TNF-α) administration elicited a more profound upregulation of P-selectin in several vascular beds, compared with wild-type and ICAM-1-deficient mice. E-selectin expression in brain of TNF-α-stimulated, ICAM-1-deficient, and P-selectin-deficient mice was attenuated compared with wild-type mice. These findings indicate that chronic deficiency of some of the adhesion glycoproteins that mediate leukocyte recruitment alters basal and induced surface expression of other adhesion molecules on endothelial cells.

Expression of Adhesion Molecules by Cultured Spiral Ligament Fibrocytes Stimulated with Proinflammatory Cytokines

2003 ◽  
Vol 112 (8) ◽  
pp. 722-728 ◽  
Author(s):  
Issei Ichimiya ◽  
Masashi Suzuki ◽  
Kazuhide Yoshida ◽  
Goro Mogi
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Proinflammatory Cytokines ◽  
Cell Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Spiral Ligament ◽  
Messenger Rnas ◽  
Tnf Α ◽  
Cell Adhesion Molecule 1

Secondary cultures from murine spiral ligament (SL) fibrocytes were stimulated with proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor–α (TNF-α), and expression of various adhesion molecules was investigated. Cultures without cytokine stimulation did not show positive immunostaining for vascular cell adhesion molecule–1 (VCAM-1), intercellular adhesion molecule–1 (ICAM-1), or mucosal addressin cell adhesion molecule–1 (MAdCAM-1). Although staining was also negative after stimulation with IL-1β, VCAM-1 and ICAM-1 staining was observed after the cells were stimulated with TNF-α. Reverse transcription-polymerase chain reaction analysis showed messenger RNAs for both VCAM-1 and ICAM-1 expression to be present after fibrocytes were stimulated with TNF-α. These data suggest that activated fibrocytes may cause inflammatory cells to persist in the SL. Given that SL fibrocytes may play a role in homeostasis of cochlear fluid and ion concentrations, prolongation of the inflammatory response could lead to fibrocyte damage that might ultimately result in cochlear malfunction.

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