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 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.

Circulating Endothelial Cell/Leukocyte Adhesion Molecules in Atherosclerosis

1994 ◽  
Vol 72 (01) ◽  
pp. 151-154 ◽  
Author(s):  
Andrew D Blann ◽  
Charles N McCollum
Keyword(s):  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Clinical Manifestations ◽  
Intercellular Adhesion Molecule ◽  
Endothelial Cell Activation ◽  
Soluble Adhesion Molecules ◽  
Von Willebrand

SummarySoluble adhesion molecules E-selectin, intercellular adhesion molecule (sICAM) and vascular cell adhesion molecule (sVCAM) were measured alongside von Willebrand factor (vWf) in 40 patients with peripheral vascular disease (PVD), 43 with ischaemic heart disease (IHD) and in equal numbers of age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0008) and in patients with PVD (p = 0.0001) relative to their respective controls but levels did not differ between the two patient groups. Raised sICAM was found in both PVD (p = 0.0003) and IHD (p = 0.0059) compared to their respective controls and was higher in PVD than in IHD (p = 0.0088). In the subjects taken as a whole, there was no correlation between vWf and sICAM. Levels of soluble E-sel-ectin and sVCAM did not differ in patients or controls. These data suggest that soluble ICAM may be useful as an index of endothelial cell activation in clinical manifestations of atherosclerosis.

Neutrophil Adhesion Molecule Expression and Serum Concentration of Soluble Adhesion Molecules during and after Pediatric Cardiovascular Surgery with or without Cardiopulmonary Bypass

2002 ◽  
Vol 96 (5) ◽  
pp. 1078-1085 ◽  
Author(s):  
Jörg Hambsch ◽  
Pavel Osmancik ◽  
József Bocsi ◽  
Peter Schneider ◽  
Attila Tárnok
Keyword(s):  
Cardiopulmonary Bypass ◽  
Serum Concentration ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cardiovascular Surgery ◽  
Interleukin 8 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Serum Concentrations ◽  
Pediatric Cardiovascular Surgery

Background Increased neutrophil activation by cardiopulmonary bypass (CPB) during cardiovascular surgery is thought to be responsible for postoperative complications. In children, the contribution of cardiovascular surgery alone to this response is not well-characterized. Methods Children undergoing surgery with CPB (CPB group, n = 35) and without CPB (control, n = 22) were studied (age, 3-17 yr). Blood was drawn 24 h preoperatively before medication, after anesthesia, after connection to CPB, at reperfusion, 4 h to 2 days after surgery, at discharge, and months after surgery. Neutrophil antigen expression and serum concentration of adhesion molecules, interleukin 8, and C5a (fragment of C5 complement) were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively. Results With and without CPB, anesthesia and surgery induced decreased LFA-1 (CD11a-CD18), Mac-1 (CD11b-CD18), CD45, and CD54 (intercellular adhesion molecule 1) surface expression and sICAM-1 serum concentrations (all P &lt; 0.001). sL-selectin serum concentration decreased with CPB (P &lt; 0.001) but was not significantly altered in the control. In contrast, CD62L expression increased during CPB (P &lt; 0.001). The time course of all analyzed markers was not significantly different between CPB and control, with the exception of sL-selectin (P = 0.017). One-day preoperative baseline values were reached days to months after surgery. Interleukin 8 and C5a serum concentrations increased after surgery in both the CPB group and the control group. Conclusions Pediatric cardiovascular surgery leads to reduced adhesiveness and activity of circulating neutrophils. This reduction is more pronounced and sustained with CPB. These data may be useful in the assessment of novel therapeutic strategies.

scholarly journals Tumor Necrosis Factor-α in Airway Secretions from Cystic Fibrosis Patients Upregulate Endothelial Adhesion Molecules and Induce Airway Epithelial Cell Apoptosis: Implications for Cystic Fibrosis Lung Disease

2008 ◽  
Vol 21 (4) ◽  
pp. 851-865 ◽  
Author(s):  
S. Mitola ◽  
V. Sorbello ◽  
E. Ponte ◽  
E. Copreni ◽  
C. Mascia ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Adhesion Molecules ◽  
Acute Exacerbation ◽  
Adhesion Molecule ◽  
Crucial Role ◽  
Adhesion Molecule Expression ◽  
Airway Epithelial ◽  
Tnf Α ◽  
Endothelial Adhesion Molecules

Airway inflammation plays a crucial role in lung damage in cystic fibrosis (CF) and is characterized by a persistent influx of neutrophils into the airways. We hypothesized that the high levels of inflammatory products that accumulate in the microenvironment of the CF lung contribute to induce the persistent neutrophil recruitment and the airway epithelial damage. Thus, we evaluated the in vitro effect of sputum sol phase (SSP) from CF patients on a) adhesion molecule expression by human microvascular endothelial cells (HMECs) and b) apoptosis of human bronchial epithelial cells (HBECs), both wild-type and CFTR-defective. SSP was obtained from 7 clinically stable adult CF patients and 8 patients with an acute exacerbation. HMECs and HBECs were cultured in the absence or presence of SSP. Cell adhesion molecule expression was assessed by flow cytometry and cell death by the detection of histone-associated DNA fragments, caspase activation, and cytochrome c release. SSP obtained from CF patients, especially at the time of an acute exacerbation, induced a) an upregulation of endothelial adhesion molecules on cultured HMECs that was associated with an increase of neutrophil adhesion to these cells, and was mediated at least in part by TNF-α and IL-1 and b) apoptosis of airway epithelial cells, mainly activated by TNF-α pathway. These results suggest that the high concentrations of inflammatory mediators in CF airways contribute both to the chronic neutrophil influx and the airway damage, and support the crucial role of early anti-inflammatory treatment in the disease.

scholarly journals Impaired microcirculatory perfusion in a rat model of cardiopulmonary bypass: the role of hemodilution

2016 ◽  
Vol 310 (5) ◽  
pp. H550-H558 ◽  
Author(s):  
Nick J. Koning ◽  
Fellery de Lange ◽  
Alexander B. A. Vonk ◽  
Yunus Ahmed ◽  
Charissa E. van den Brom ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Adhesion Molecule ◽  
Rat Model ◽  
Renal Injury ◽  
Tissue Injury ◽  
Multiple Time ◽  
Adhesion Molecule Expression ◽  
Microcirculatory Perfusion ◽  
Endothelial Adhesion Molecule ◽  
Sham Procedure

Although hemodilution is attributed as the main cause of microcirculatory impairment during cardiopulmonary bypass (CPB), this relationship has never been investigated. We investigated the distinct effects of hemodilution with or without CPB on microvascular perfusion and subsequent renal tissue injury in a rat model. Male Wistar rats (375–425 g) were anesthetized, prepared for cremaster muscle intravital microscopy, and subjected to CPB ( n = 9), hemodilution alone ( n = 9), or a sham procedure ( n = 6). Microcirculatory recordings were performed at multiple time points and analyzed for perfusion characteristics. Kidney and lung tissue were investigated for mRNA expression for genes regulating inflammation and endothelial adhesion molecule expression. Renal injury was assessed with immunohistochemistry. Hematocrit levels dropped to 0.24 ± 0.03 l/l and 0.22 ± 0.02 l/l after onset of hemodilution with or without CPB. Microcirculatory perfusion remained unaltered in sham rats. Hemodilution alone induced a 13% decrease in perfused capillaries, after which recovery was observed. Onset of CPB reduced the perfused capillaries by 40% (9.2 ± 0.9 to 5.5 ± 1.5 perfused capillaries per microscope field; P < 0.001), and this reduction persisted throughout the experiment. Endothelial and inflammatory activation and renal histological injury were increased after CPB compared with hemodilution or sham procedure. Hemodilution leads to minor and transient disturbances in microcirculatory perfusion, which cannot fully explain impaired microcirculation following cardiopulmonary bypass. CPB led to increased renal injury and endothelial adhesion molecule expression in the kidney and lung compared with hemodilution. Our findings suggest that microcirculatory impairment during CPB may play a role in the development of kidney injury.

scholarly journals Targeting Endothelial Adhesion Molecule Transcription for Treatment of Inflammatory Disease: A Proof-of-Concept Study

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Liam M. Ashander ◽  
Binoy Appukuttan ◽  
Yuefang Ma ◽  
Dione Gardner-Stephen ◽  
Justine R. Smith
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Inflammatory Disease ◽  
Leukocyte Migration ◽  
Proof Of Concept ◽  
Physiological Level ◽  
Endothelial Adhesion Molecule ◽  
Concept Study ◽  
Endothelial Adhesion Molecules

Targeting the endothelial adhesion molecules that control leukocyte trafficking into a tissue has been explored as a biological therapy for inflammatory diseases. However, these molecules also participate in leukocyte migration for immune surveillance, and inhibiting the physiological level of an adhesion molecule might promote infection or malignancy. We explored the concept of targeting endothelial adhesion molecule transcription during inflammation in a human system. Intercellular adhesion molecule 1 (ICAM-1) mediates leukocyte migration across the retinal endothelium in noninfectious posterior uveitis. We observed an increase in the transcription factor, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NF-κB1), in parallel with ICAM-1, in human retinal endothelial cells treated with tumor necrosis factor-alpha (TNF-α), and identified putative binding sites for NF-κB1 within theICAM-1regulatory region. We targeted induced NF-κB1 expression in endothelial cells with small interfering (si)RNA. Knockdown of NF-κB1 significantly decreased cell surface expression of ICAM-1 protein induced by TNF-αbut did not reduce constitutive ICAM-1 expression. Consistently, NF-κB1 knockdown significantly reduced leukocyte binding to cell monolayers in the presence of TNF-αbut did not impact baseline binding. Findings of this proof-of-concept study indicate that induced transcription of endothelial adhesion molecules might be targeted therapeutically for inflammatory disease in humans.

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