scholarly journals Role of glucocorticoids in neutrophil and endothelial adhesion molecule expression and function

1992 ◽  
Vol 1 (2) ◽  
pp. 101-106 ◽  
Author(s):  
Kevin D. Forsyth ◽  
Vivienne Talbot
Keyword(s):  
Inflammatory Response ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Antigen Expression ◽  
Neutrophil Adhesion ◽  
Adhesion Molecule Expression ◽  
Chronic Inflammatory Response ◽  
Endothelial Adhesion Molecule ◽  
And Function

Glucocorticoids are very effective inhibitors of both the acute and chronic inflammatory response. In this study the hypothesis that glucocorticoids inhibit an early component of the inflammatory response, neutrophil adhesion to endothelium, by down-regulation of adhesion molecules on neutrophils or endothelium was examined. No effect of dexamethasone on neutrophil adhesion to endothelium or of antigen expression by neutrophils or endothelium was found. The mechanism of action of glucocorticoids in the inflammatory response is probably not mediated by alterations in adhesion molecules.

scholarly journals Endothelial Adhesion Molecule Expression and Its Inhibition by Recombinant Bactericidal/Permeability-Increasing Protein Are Influenced by the Capsulation and Lipooligosaccharide Structure ofNeisseria meningitidis

1999 ◽  
Vol 67 (11) ◽  
pp. 5626-5633 ◽  
Author(s):  
Garth L. J. Dixon ◽  
Robert S. Heyderman ◽  
Karolena Kotovicz ◽  
Dominic L. Jack ◽  
Svein R. Andersen ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neisseria Meningitidis ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Meningococcal Disease ◽  
Clinical Manifestations ◽  
Adhesion Molecule Expression ◽  
Central Process ◽  
Potent Inducer ◽  
Endothelial Adhesion Molecule

ABSTRACT Vascular endothelial injury is responsible for many of the clinical manifestations of severe meningococcal disease. Binding and migration of activated host inflammatory cells is a central process in vascular damage. The expression and function of adhesion molecules regulate interactions between leukocytes and endothelial cells. Little is known about how meningococci directly influence these receptors. In this study we have explored the effect of Neisseria meningitidison endothelial adhesion molecule expression and found this organism to be a potent inducer of the adhesion molecules CD62E, ICAM-1, and VCAM-1. Exposure of endothelium to a serogroup B strain ofNeisseria meningitidis, B1940, and a range of isogenic mutants revealed that lipooligosaccharide (LOS) structure and capsulation influence the expression of adhesion molecules. Following only a brief exposure (15 min) to the bacteria, there were large differences in the capacity of the different mutants to induce vascular cell adhesion molecules, with the unencapsulated and truncated LOS strains being most potent (P < 0.05). Furthermore, the pattern of cell adhesion molecule expression was different with purified endotoxin from that with intact bacteria. Meningococci were more potent stimuli of CD62E expression than was endotoxin, whereas endotoxin was at least as effective as meningococci in inducing ICAM-1 and VCAM-1. The effect of bactericidal/permeability increasing protein (rBPI21), an antibacterial molecule with antiendotoxin properties, was also dependent on LOS structure. The strains which possessed a truncated or nonsialylated LOS, whether capsulated or not, were more sensitive to the inhibitory effects of rBPI21. These findings could have important implications for the use of antiendotoxin therapy in meningococcal disease.

Inhibition of phorbol ester-induced cellular adhesion by competitive binding of NF-kappa B in vivo

1993 ◽  
Vol 13 (10) ◽  
pp. 6530-6536
Author(s):  
S L Eck ◽  
N D Perkins ◽  
D P Carr ◽  
G J Nabel
Keyword(s):  
Transcription Factor ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cellular Adhesion ◽  
Adhesion Molecule Expression ◽  
Nf Kappa B ◽  
Induced Differentiation ◽  
And Function

Adhesive interactions between cells are essential for the organization and function of differentiated tissues and organs and are mediated by inducible cell surface glycoproteins. In normal tissues, cell adhesion molecules contribute to immune regulation, inflammation, and embryogenesis. Additionally, they play an important role in a variety of pathogenic processes. Cell adhesion molecule expression can be induced by stimuli known to activate NF-kappa B, a ubiquitous transcription factor found in a variety of cell types. To investigate the role of NF-kappa B in cell adhesion molecule expression, we treated HL-60 cells with a double-stranded oligonucleotide which specifically inhibits NF-kappa B-mediated transcription. This treatment resulted in the inhibition of phorbol 12-myristate 13-acetate (PMA)-induced cellular adhesion, morphological changes, and the expression of leukocyte integrin CD11b. In a similar fashion, expression of intercellular adhesion molecule 1 on human endothelial cells induced by PMA was specifically inhibited by the NF-kappa B antagonist. We suggest that NF-kappa B activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain adhesion molecules. Furthermore, the inhibition of transcription factor functions by this generally applicable mechanism can be used to define their role in cellular differentiation and function.

Expression of soluble endothelial adhesion molecules in clinical cardiopulmonary bypass

Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 314-321 ◽  
Author(s):  
Joseph Galea ◽  
Naomi Rebuck ◽  
Adam Finn ◽  
Alex Manché ◽  
Neil Moat
Keyword(s):  
Cardiopulmonary Bypass ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Control Group ◽  
Adhesion Molecule Expression ◽  
Endothelial Cell Activation ◽  
Endothelial Adhesion Molecule ◽  
Endothelial Adhesion Molecules ◽  
Serial Measurements

Soluble endothelial adhesion molecule expression in clinical cardiopulmonary bypass (CPB) was investigated. Neutrophil-mediated endothelial injury plays an important role in CPB-induced organ dysfunction. The adhesion of neutrophil to the endothelium is central to this process. It has been well documented that CPB induces neutrophil activation and changes in neutrophil adhesion molecule expression, but the effect of CPB on endothelial cell activation is not known. This study was designed to measure soluble endothelial adhesion molecules during CPB. We made serial measurements (by specific enzyme-linked immunoabsorbent assay) of plasma levels of the soluble endothelial adhesion molecules, ICAM-1 and E-selectin in patients undergoing routine CPB ( n =7) and in a control group (thoracotomy, n = 3). The results show an initial significant decrease during CPB followed by an increase in plasma E-selectin from 29.3 ± 5.1 ng/ml (mean ± SEM) prebypass to 34.0 ± 5.4 ng/ml at 48 h postbypass. Likewise, plasma ICAM-1 significantly decreased during CPB and then increased from 246.3 ± 38.0 ng/ml before bypass to 324.8 ± 25.0 ng/ml and 355.0 ± 23.0 ng/ml at 24 and 48 h after bypass, respectively. The rise in levels is statistically significant ( p < 0.05). This study shows a decrease in circulating ICAM-1 and soluble E-selectin during CPB and an increase in their levels at 48 h after CPB.

scholarly journals Inhibition of phorbol ester-induced cellular adhesion by competitive binding of NF-kappa B in vivo.

1993 ◽  
Vol 13 (10) ◽  
pp. 6530-6536 ◽  
Author(s):  
S L Eck ◽  
N D Perkins ◽  
D P Carr ◽  
G J Nabel
Keyword(s):  
Transcription Factor ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cellular Adhesion ◽  
Adhesion Molecule Expression ◽  
Nf Kappa B ◽  
Induced Differentiation ◽  
And Function

Adhesive interactions between cells are essential for the organization and function of differentiated tissues and organs and are mediated by inducible cell surface glycoproteins. In normal tissues, cell adhesion molecules contribute to immune regulation, inflammation, and embryogenesis. Additionally, they play an important role in a variety of pathogenic processes. Cell adhesion molecule expression can be induced by stimuli known to activate NF-kappa B, a ubiquitous transcription factor found in a variety of cell types. To investigate the role of NF-kappa B in cell adhesion molecule expression, we treated HL-60 cells with a double-stranded oligonucleotide which specifically inhibits NF-kappa B-mediated transcription. This treatment resulted in the inhibition of phorbol 12-myristate 13-acetate (PMA)-induced cellular adhesion, morphological changes, and the expression of leukocyte integrin CD11b. In a similar fashion, expression of intercellular adhesion molecule 1 on human endothelial cells induced by PMA was specifically inhibited by the NF-kappa B antagonist. We suggest that NF-kappa B activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain activation is a necessary event for the PMA-induced differentiation of HL-60 cells and the expression of certain adhesion molecules. Furthermore, the inhibition of transcription factor functions by this generally applicable mechanism can be used to define their role in cellular differentiation and function.

scholarly journals Calmodulin Regulates L-Selectin Adhesion Molecule Expression and Function through a Protease-Dependent Mechanism

Cell ◽  
1998 ◽  
Vol 92 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Julius Kahn ◽  
Bruce Walcheck ◽  
Grace I Migaki ◽  
Mark A Jutila ◽  
Takashi Kei Kishimoto
Keyword(s):  
Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
And Function ◽  
Dependent Mechanism

Neutrophil adhesion molecule expression during cardiopulmonary bypass with bubble and membrane oxygenators

1993 ◽  
Vol 56 (4) ◽  
pp. 847-853 ◽  
Author(s):  
A.Marc Gillinov ◽  
Jenny M. Bator ◽  
Kenton J. Zehr ◽  
J.Mark Redmond ◽  
Ronald M. Burch ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Adhesion Molecule ◽  
Neutrophil Adhesion ◽  
Adhesion Molecule Expression ◽  
Membrane Oxygenators
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