Immune Regulation by Platelet-Activating Factor: II. Mediation of Suppression by Cytokine-Stimulated Endothelial Cells In Vitro

1991 ◽  
Vol 49 (3) ◽  
pp. 245-252 ◽  
Author(s):  
Chantal Lacasse ◽  
Marek Rola-Pleszczynski
Keyword(s):  
Endothelial Cells ◽  
Immune Regulation ◽  
Platelet Activating Factor ◽  
Factor Ii

scholarly journals P-selectin and platelet-activating factor mediate initial endotoxin-induced neutropenia.

1994 ◽  
Vol 179 (1) ◽  
pp. 329-334 ◽  
Author(s):  
A F Coughlan ◽  
H Hau ◽  
L C Dunlop ◽  
M C Berndt ◽  
W W Hancock
Keyword(s):  
Endothelial Cells ◽  
Platelet Activating Factor ◽  
Surface Expression ◽  
Rapid Onset ◽  
In Vivo Studies ◽  
Polymorphonuclear Neutrophil ◽  
Initial Adhesion ◽  
Kidney Liver

Polymorphonuclear neutrophil (PMN) accumulation within damaged tissues, a hallmark of acute inflammation, is dependent upon initial adhesion to endothelial cells. In vitro studies suggest that P-selectin and platelet activating factor (PAF) are key molecules in this process by promoting the initial adhesion of PMN to endothelial cells. We report in vivo studies in which intravenous administration of lipopolysaccharide (LPS) to anesthetized rats caused a very rapid onset (< 5 min) of neutropenia, in association with induction of surface expression of P-selectin on microvascular endothelial cells in kidney, liver and lung; analogous induction of P-selectin expression by cultured endothelial cells was observed in response to LPS stimulation in vitro. In addition, treatment with an antibody (Ab) to P-selectin (or use of a PAF antagonist) blocked development of neutropenia in vivo for at least 15 min post-LPS injection, and Ab treatment was shown to block PMN accumulation in tissues. These studies document roles for P-selectin and PAF in the early adhesion of PMN to endothelial cells in vivo.

Adhesion of flowing neutrophils to cultured endothelial cells after hypoxia and reoxygenation in vitro

1995 ◽  
Vol 269 (4) ◽  
pp. H1398-H1406 ◽  
Author(s):  
G. E. Rainger ◽  
A. Fisher ◽  
C. Shearman ◽  
G. B. Nash
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Platelet Activating Factor ◽  
Neutrophil Recruitment ◽  
Severe Hypoxia ◽  
Adhesion Assay ◽  
Endothelial Response ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells

Using a novel in-line deoxygenating system linked to an in vitro flow-based adhesion assay and video microscopy, we have studied neutrophil recruitment and migration after hypoxia and reoxygenation of cultured human umbilical vein endothelial cells (HUVEC). Unstimulated purified neutrophils were perfused over reoxygenating HUVEC immediately after various periods of endothelial hypoxia. Adhesion to HUVEC was dependent on the duration of hypoxia, with 30, 60, and 100 min of exposure causing graded increments in neutrophil recruitment. The degree of hypoxia also markedly influenced the endothelial response. Severe hypoxia (O2 < 2.5%) induced stationary attachment and then migration of neutrophils, in contrast to rolling adhesion alone under a less intense regime (O2 = 2.5-4.0%). Judged from studies with monoclonal antibodies, P-selectin was essential for adhesion after severe hypoxia, and neutrophil immobilization was attributable to the activation of neutrophil beta 2-integrin. Perfusion of neutrophils with an antibody against interleukin-8 or a platelet-activating factor antagonist reduced levels of adhesion. However, IL-8 appeared to be the dominant agent involved in the immobilization from flow, whereas platelet-activating factor was the more potent agent involved in initiating subendothelial migration. Thus endothelial cells alone can initiate all stages of adhesion and migration of flowing neutrophils after hypoxia and reperfusion.

ω-3 Fatty acids suppress monocyte adhesion to human endothelial cells: role of endothelial PAF generation

2002 ◽  
Vol 283 (2) ◽  
pp. H811-H818 ◽  
Author(s):  
Konstantin Mayer ◽  
Martina Merfels ◽  
Marion Muhly-Reinholz ◽  
Stephanie Gokorsch ◽  
Simone Rosseau ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Platelet Activating Factor ◽  
Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Umbilical Vein Endothelial Cells

Monocyte-endothelium interaction is a fundamental process in many acute and chronic inflammatory diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are fish oil-derived alternative (ω-3) precursor fatty acids implicated in the suppression of inflammatory events. We investigated their influence on rolling and adhesion of monocytes to human umbilical vein endothelial cells (HUVEC) under laminar flow conditions in vitro. Exposure of HUVEC to tumor necrosis factor (TNF-α) strongly increased 1) surface expression of intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and E-selectin, 2) platelet-activating factor (PAF) synthesis as assessed by thrombin challenge, and 3) rate of rolling and adhesion of monocytes. Preincubation of HUVEC with EPA or DHA markedly suppressed PAF synthesis, monocyte rolling, and adherence, whereas expression of endothelial adhesion molecules was unchanged. Also, PAF receptor antagonists markedly suppressed the adhesion rate of monocytes, and EPA or DHA revealed no additional inhibitory capacity. In contrast, arachidonic acid partially reversed the effect of the antagonist. We conclude that ω-3 fatty acids suppress rolling and adherence of monocytes on activated endothelial cells in vitro by affecting endothelial PAF generation.

scholarly journals Effect of rose extract treatment on soluble CCR5 and CXCR4 secretion by the endothelial cells in vitro

2021 ◽  
Vol 8 (5) ◽  
pp. 4333-4344
Author(s):  
Mark Christopher Arokiaraj ◽  
Eric Menesson
Keyword(s):  
Endothelial Cells ◽  
Immune Regulation ◽  
Novel Therapy ◽  
Physiological Conditions ◽  
Elisa Technique ◽  
Huvec Cells ◽  
Clinical Conditions ◽  
Cc Chemokine Receptor 5 ◽  
The Rose

Background: CC-Chemokine Receptor 5 (CCR5) and Chemokine C-X-C-Motif Receptor 4 (CXCR4) are expressed in various tissues, and they are potential molecules involved in multiple pathways. CCR5 and CXCR4 targets are associated with immune regulation in patients in multiple tissues and numerous clinical conditions. The study was performed searching for a novel therapy for immune regulation on these CCR5 and CXCR4 receptors with rose extract. Methods: The crushed red rose extract was prepared, and it was processed for analysis. The HUVEC cells were obtained for seeding in the cell culture. The cells were tested in normal physiological conditions and varying degrees of hypoxia. The cells were treated with extract for 72 hours, and the resultant secreted supernatants were analyzed for expression of CCR5 and CXCR4 by the Elisa technique. Results: The CCR5 levels were significantly elevated at normoxia compared to untreated controls. The surge of CCR5 was persistent in 12% hypoxia, and at higher degrees of hypoxia, the levels were mildly lower than the untreated levels. The CXCR4 levels were not changed in normoxia, and even with significant hypoxia, the levels were similar or mildly reduced compared to untreated values. Conclusion: The rose extract has the potentials to induce the secretion of soluble CCR5 from the HUVEC cells, and it can prevent the reduction of soluble CXCR4 levels during the hypoxic challenge of the endothelial cells. This in-turn can modulate the receptor levels on the endothelial cells, which has clinical applications.

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