Altered Adhesion Molecule Expression and Endothelial Cell Activation Accompany the Recruitment of Human Granulocytes to the Lung after Segmental Antigen Challenge

1992 ◽  
Vol 7 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Steve N. Georas ◽  
Mark C. Liu ◽  
Walter Newman ◽  
L. Dawson Beall ◽  
Becky A. Stealey ◽  
...  
Blood ◽  
2014 ◽  
Vol 123 (3) ◽  
pp. 377-390 ◽  
Author(s):  
John D. Belcher ◽  
Chunsheng Chen ◽  
Julia Nguyen ◽  
Liming Milbauer ◽  
Fuad Abdulla ◽  
...  

Key Points Heme, released from hemoglobin, elicits vaso-occlusion in transgenic sickle mice via endothelial TLR4 signaling. Heme/TLR4 signaling activates NF-κB and triggers vaso-occlusion through Weibel-Palade body degranulation and adhesion molecule expression.


2004 ◽  
Vol 286 (5) ◽  
pp. C1195-C1202 ◽  
Author(s):  
Peter J. Kuhlencordt ◽  
Eva Rosel ◽  
Robert E. Gerszten ◽  
Manuel Morales-Ruiz ◽  
David Dombkowski ◽  
...  

The objective of this study was to determine whether absence of endothelial nitric oxide synthase (eNOS) affects the expression of cell surface adhesion molecules in endothelial cells. Murine lung endothelial cells (MLECs) were prepared by immunomagnetic bead selection from wild-type and eNOS knockout mice. Wild-type cells expressed eNOS, but eNOS knockout cells did not. Expression of neuronal NOS and inducible NOS was not detectable in cells of either genotype. Upon stimulation, confluent wild-type MLECs produced significant amounts of NO compared with Nω-monomethyl-l-arginine-treated wild-type cells. eNOS knockout and wild-type cells showed no difference in the expression of E-selectin, P-selectin, intracellular adhesion molecule-1, and vascular cell adhesion molecule-1 as measured by flow cytometry on the surface of platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31)-positive cells. Both eNOS knockout and wild-type cells displayed the characteristics of resting endothelium. Adhesion studies in a parallel plate laminar flow chamber showed no difference in leukocyte-endothelial cell interactions between the two genotypes. Cytokine treatment induced endothelial cell adhesion molecule expression and increased leukocyte-endothelial cell interactions in both genotypes. We conclude that in resting murine endothelial cells, absence of endothelial production of NO by itself does not initiate endothelial cell activation or promote leukocyte-endothelial cell interactions. We propose that eNOS derived NO does not chronically suppress endothelial cell activation in an autocrine fashion but serves to counterbalance signals that mediate activation.


1994 ◽  
Vol 72 (01) ◽  
pp. 151-154 ◽  
Author(s):  
Andrew D Blann ◽  
Charles N McCollum

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.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3310-3310
Author(s):  
Xiaojin Sha ◽  
Shu Meng ◽  
Xinyuan Li ◽  
Jahaira Lopez Pastrana ◽  
Hong Wang ◽  
...  

Abstract Abstract 3310 Our previous reports showed that survival/apoptosis of CD4+CD25+Foxp3+ regulatory T cells (Tregs) modulates vascular inflammation even though the mode of Tregs inhibition was unknown. Interleukin-35 (IL-35), consisting of two subunits Epstein-Barr virus–induced gene 3 (EBI3) and p35, is a novel anti-inflammatory cytokine, which is a member of the interleukin-12 (IL-12) cytokine family. IL-35 is produced by Tregs. It has been shown that IL-35 suppresses chronic inflammatory diseases such as asthma and inflammatory bowel diseases. However, an important question of whether IL-35 can carry out Tregs suppression and inhibit endothelial cell (EC) activation in acute inflammation remained unknown. Here we found that IL-35 significantly inhibits lung neutrophil infiltration into the surrounding areas of bronchioles and alveolar space when induced by intraperitoneal injection of lipopolysaccharide (LPS) in wild type mice and EBI3-deficient mice. Furthermore, cremaster microvasculature study using intravital microscopy showed IL-35 significantly suppresses leukocyte adhesion to the vascular wall as well, suggesting IL-35 inhibition of endothelial activation. Mechanistically, IL-35 inhibited LPS-induced upregulation of adhesion molecules on human aortic endothelial cells, a marker of endothelial activation, including vascular cell adhesion molecule 1 (VCAM-1). IL-35 acted through new IL-35 dimeric receptors gp130 and IL-12Rβ2, and inhibited VCAM-1 promoter transcription in mitogen-activated protein kinase (MAPK)-mediated pathway. These results provide a novel insight on Tregs and IL-35 inhibition of vascular inflammation. Disclosures: No relevant conflicts of interest to declare.


2005 ◽  
Vol 103 (4) ◽  
pp. 759-767 ◽  
Author(s):  
Boris Nohé ◽  
Tanja Johannes ◽  
Jörg Reutershan ◽  
Albert Rothmund ◽  
Helene A. Haeberle ◽  
...  

Background It has been suspected that synthetic colloids may interfere with leukocyte adhesion by down-regulation of endothelial cell adhesion molecules. Although inhibition of endothelial inflammation might reduce leukocyte-related tissue injury, the same mechanism may be detrimental for host defense during severe infection. Regarding the widespread use of colloids, the authors performed a laboratory investigation to determine the mechanisms by which synthetic colloids interfere with leukocyte-endothelial interactions. Methods Adhesion molecule expression on native and cytokine-activated endothelium from umbilical veins was measured after pretreatment with gelatin and various preparations of dextran or hydroxyethyl starch. Inhibition of neutrophil adhesion to activated endothelium was examined in a flow chamber by perfusion of untreated and colloid-treated neutrophils over colloid-pretreated endothelium at 2 dyn/cm. Comparisons were made between untreated controls, colloid-pretreated endothelium, and colloid-cotreated neutrophils. Results Intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and P-selectin were not attenuated by any colloid. Accordingly, colloid pretreatment of endothelium alone did not reduce neutrophil adhesion. In contrast, when neutrophils were cotreated by addition of colloids to the perfusate immediately before perfusion, adhesion decreased by 31-51% (P < 0.05) regardless of the colloid type. As indicated by the twofold increased rolling fractions, this reduction was due to an inhibition of neutrophil integrins. Conclusions This study shows that synthetic colloids inhibit neutrophil adhesion by a neutrophil-dependent mechanism rather than interfering with endothelial cell activation. This suggests that inhibition of leukocyte sequestration by volume support is a common and transient phenomenon depending on the colloid concentration in plasma.


Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 314-321 ◽  
Author(s):  
Joseph Galea ◽  
Naomi Rebuck ◽  
Adam Finn ◽  
Alex Manché ◽  
Neil Moat

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.


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