## Abstract We investigated the effect of prostaglandin E1 on human polymorphonuclear leukocytes, __in vivo__. Polymorphonuclear leukocytes of a prostaglandin E1 and placebo study group were harvested and their function, as production of oxygen‐derived metabolites and adherence to human cultured en
Simultaneous measurement of endothelial cell damage, elastase release and chemiluminescence response during interaction between polymorphonuclear leukocytes and endothelial cells
✍ Scribed by Jonas, Eleonore ;Dwenger, Alexander ;Lueken, Britta ;Boehme, Ulrich
- Publisher
- John Wiley and Sons
- Year
- 1991
- Weight
- 650 KB
- Volume
- 6
- Category
- Article
- ISSN
- 0884-3996
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✦ Synopsis
Using cultured human umbilical cord vein endothelial cells and human blood neutrophils, the interaction between neutrophils and endothelial cells, in vitro, was studied. The aim of the study was t o examine whether a respiratory burst stimulation by neutrophils would be observed by neutrophil/endothelial cell interaction and whether the respiratory burst stimulation of neutrophils by endothelial cells could be enhanced by lipopolysaccharide stimulation o f neutrophils. The second aim was whether such an effect, or secretion of elastase, could cause a n endothelial cell damage in vitro.
Chemiluminescence as an indicator of oxygen-derived metabolites produced by neutrophils, elastase release by neutrophils, and endothelial cell damage, based on "'
In-oxine release from labelled endothelial cells, were measured simultaneously. The present investigation demonstrates that neutrophils can be directly stimulated by endothelial cells. A further amplification of this process following lipopolysaccharide priming up t o 10 ng/ml blood could be demonstrated. A slight endothelial cell damage occurs following neutrophil stimulation, although elastase secretion does not increase during interaction between neutrophils and endothelial cells. These results raise the possibility that oxygen-derived metabolites rather than elastase contribute t o an endothelial cell damage which might occur in conditions such as endotoxin-induced adult respiratory distress syndrome.
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