scholarly journals Avena Rhealba® Inhibits A23187-Stimulated Arachidonic Acid Mobilization, Eicosanoid Release, and cPLA2 Expression in Human Keratinocytes: Potential in Cutaneous Inflammatory Disorders

2005 ◽  
Vol 28 (4) ◽  
pp. 601-606 ◽  
Author(s):  
Marie-Françoise Aries ◽  
Clémence Vaissiere ◽  
Eric Pinelli ◽  
Bernard Pipy ◽  
Marie Charveron
Keyword(s):  
Arachidonic Acid ◽  
Human Keratinocytes ◽  
Inflammatory Disorders ◽  
Eicosanoid Release

scholarly journals Cyclic-AMP mediated drugs: differential or global reduction of eicosanoid synthesis in the isolated rat lung?

1992 ◽  
Vol 1 (4) ◽  
pp. 255-261
Author(s):  
Mark J. Post ◽  
Jan Dirk te Biesebeek ◽  
Johan Wemer ◽  
Hans H. van Rooij ◽  
Freek J. Zijlstra ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Rat Lung ◽  
Eicosanoid Synthesis ◽  
Eicosanoid Release ◽  
Isolated Lungs ◽  
A Site ◽  
Isolated Rat Lung ◽  
Global Reduction

In this study the question was addressed whether cAMP mediated drugs induce a differential reduction of branches of the arachidonic acid metabolism rather than a global reduction of eicosanoid synthesis. The isolated lungs of actively sensitized rats were employed to study prostaglandin and leukotriene release in the presence and absence of the cAMP mediated drugs theophylline, milrinone, sulmazole, isobutyl-methylxanthine and salbutamol. The release of eicosanoids as measured by RIA was predominantly basal and continuous, with a mild antigen induced stimulation only for TXB2and the leukotrienes. All drugs reduced eicosanoid release globally. It is concluded that cAMP mediated drugs interfere with arachidonic acid metabolism at a site proximal to the branching into lipoxygenase and cyclo-oxygenase pathways.

Influence of growth oxygen level on eicosanoid release from lung endothelial cells during hypoxia

1992 ◽  
Vol 263 (4) ◽  
pp. L454-L459
Author(s):  
W. E. Holden ◽  
E. M. Burnham ◽  
M. A. Lee ◽  
S. P. Bagby
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Acute Hypoxia ◽  
Calcium Ionophore ◽  
Pulmonary Vasculature ◽  
Ionophore A23187 ◽  
Oxygen Level ◽  
Arachidonic Acid Release ◽  
Eicosanoid Release ◽  
Acid Release

Eicosanoid products of arachidonic acid are suspected modulators of hypoxic vasoconstriction in the pulmonary vasculature. Vascular endothelial cells (EC) release several eicosanoids, but there is disagreement regarding the effect of hypoxia on EC eicosanoid release. We postulated that the oxygen level of growth in culture might influence the release of eicosanoids during acute hypoxia. We studied EC cultured from the main pulmonary arteries of pigs and grown at either 5% or near 20% oxygen, representing the normal limits of oxygen exposure to endothelium in normal lungs. Although cultures grown in 5% oxygen grew slightly faster by 4 days, the confluent cell number, protein content, and baseline eicosanoid release were no different compared with paired cultures grown in 20% oxygen. However, with an acute decrease in oxygen level, cultures grown in 5% oxygen released less prostaglandin E2, F2 alpha, and 6-ketoprostaglandin F1 alpha compared with amounts released at the growth oxygen level. In contrast, cultures grown in 20% oxygen released increased amounts of these eicosanoids compared with release at the growth oxygen level. Release of thromboxane B2 was not significantly different during hypoxia between cultures grown at 5% vs. 20% oxygen. In other experiments, cyclooxygenase activity, stimulated arachidonic acid release by calcium ionophore A23187, and uptake of arachidonic acid were no different in cultures grown at 5% vs. 20% oxygen. However, arachidonic acid release during hypoxia was reduced in 5% cultures and increased in 20% cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Production of arachidonic acid metabolites in adult rat cardiac myocytes, endothelial cells, and fibroblast-like cells

1993 ◽  
Vol 264 (3) ◽  
pp. H973-H982 ◽  
Author(s):  
M. C. Linssen ◽  
W. Engels ◽  
P. J. Lemmens ◽  
V. V. Heijnen ◽  
M. Van Bilsen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
High Performance ◽  
Cellular Protein ◽  
Ionophore A23187 ◽  
Adult Rat ◽  
Eicosanoid Release ◽  
Stable Product ◽  
Acid Metabolites ◽  
Pg E2

Cells were incubated in the presence of the Ca2+ ionophore A23187 (10 microM) and arachidonic acid (AA, 80 microM). The release of eicosanoids from subcultivated cardiac endothelial and fibroblast-like cells amounted to 23.3 +/- 4.5 and 2.0 +/- 0.4 nmol/mg cellular protein per 30 min, respectively. The release from isolated cardiomyocytes remained below the detection limit of the high-performance liquid chromatography assay (< 0.00015 nmol/assay). When a very sensitive radioimmunoassay was applied, cardiomyocytes released 0.002 +/- 0.0001 nmol prostacyclin per milligram cellular protein per 30 min. Prostaglandin (PG) E2 and PGF2 alpha, 12-hydroxyheptadecatrienoic acid, 11- and 15-hydroxyeicosatetraenoic acid, and thromboxane B2 were the main eicosanoids released by endothelial cells. The stable product of prostacyclin, 6-keto-PGF1 alpha, contributed relatively little to the total amount of eicosanoids formed by endothelial cells. Fibroblast-like cells released predominantly PGE2 and 6-keto-PGF1 alpha and, to a lesser extent, 12-hydroxyheptadecatrienoic and 15-hydroxyeicosatetraenoic acids. Neither endothelial cells nor fibroblast-like cells released leukotrienes. A23187 stimulated eicosanoid release from endothelial cells when exogenous AA was below 40 microM. Addition of albumin reduced the amount of eicosanoids produced. Histamine and bradykinin did not influence 6-keto-PGF1 alpha and PGE2 production in cardiomyocytes. Histamine only gave rise to a slight but significantly higher release of 6-keto-PGF1 alpha in endothelial cells.

Differential Utilization of Linoleic and Arachidonic Acid by Cultured Human Keratinocytes

1995 ◽  
Vol 8 (1-2) ◽  
pp. 30-40 ◽  
Author(s):  
Nanna Schürer ◽  
Viola Schliep ◽  
Mary L. Williams
Keyword(s):  
Arachidonic Acid ◽  
Human Keratinocytes

scholarly journals Bacterial Challenge Stimulates Formation of Arachidonic Acid Metabolites by Human Keratinocytes and Neutrophils In Vitro

2002 ◽  
Vol 9 (1) ◽  
pp. 132-137 ◽  
Author(s):  
Jörg Eberhard ◽  
Søren Jepsen ◽  
Lutz Pohl ◽  
Hans Karl Albers ◽  
Yahya Açil
Keyword(s):  
Immune Response ◽  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Pathogenic Bacteria ◽  
Human Keratinocytes ◽  
Human Neutrophils ◽  
Prostaglandin E ◽  
Bacterial Challenge ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

ABSTRACT Although the interactions of bacteria with keratinocytes induce the synthesis of various mediators, the capability of epithelial cells to form arachidonic acid mediators has not been studied, and therefore the first part of this study was initiated. The complex mixture of epithelium-derived mediators suggests that chemoattraction is not their only effect on neutrophils and that they may also affect neutrophil mediator synthesis. The effect of epithelium-derived mediators on neutrophil eicosanoide synthesis was evaluated in the second part of this study. We incubated human keratinocytes with human-pathogenic bacteria for 2 h and harvested the supernatants after 4, 6, 10, and 18 h of culture. Subsequently, the supernatants were coincubated for 5 min with human neutrophils with or without arachidonic acid. The formation of the arachidonic acid metabolites prostaglandin E2 (PGE2), leukotriene B4 (LTB4), 12-hydroxyeicosatetraenoic acid (12-HETE), and 15-HETE in keratinocytes and neutrophils was measured by reverse-phase high-pressure liquid chromatography. We demonstrated for the first time that keratinocytes produced significant amounts of LTB4 and 12-HETE 4 to 6 h after bacterial challenge. Upon stimulation with epithelial supernatants, neutrophils produced significant amounts of PGE2, LTB4, 12-HETE, and 15-HETE throughout the observation period of 18 h, with a maximum synthesis by supernatants harvested 4 to 10 h after bacterial infection. The results of the study suggest that arachidonic acid mediator formation by epithelial cells following bacterial challenge may act as an early inflammatory signal for the initiation of the immune response. The epithelial supernatants were capable of inducing the formation of arachidonic acid mediators by neutrophils, which may have further regulatory effects on the immune response.

Sign in / Sign up

Export Citation Format

Share Document