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https://hdl.handle.net/2440/7502
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Type: | Journal article |
Title: | Unique effect of arachidonic acid on human neutrophil TNF receptor expression: Up-regulation involving protein kinase C, extracellular signal-regulated kinase, and phospholipase A₂¹ |
Other Titles: | Unique effect of arachidonic acid on human neutrophil TNF receptor expression: Up-regulation involving protein kinase C, extracellular signal-regulated kinase, and phospholipase A(2)(1) |
Author: | Moghaddami, N. Costabile, M. Grover, P. Jersmann, H. Huang, Z. Hii, C. Ferrante, A. |
Citation: | Journal of Immunology, 2003; 171(5):2616-2624 |
Publisher: | Amer Assoc Immunologists |
Issue Date: | 2003 |
ISSN: | 0022-1767 1550-6606 |
Statement of Responsibility: | Nahid Moghaddami, Maurizio Costabile, Phulwinder K. Grover, Hubertus P. A. Jersmann, Zhi H. Huang, Charles S. T. Hii, and Antonio Ferrante |
Abstract: | Arachidonic acid (AA) regulates the function of many cell types, including neutrophils. Although much emphasis has been placed on agonist-induced down-regulation of TNFR, our data show that AA caused a rapid (10–20 min) and dose-dependent (0.5–30 µM) increase in the surface expression of both classes of TNFR (TNFR1 and TNFR2) on human neutrophils. This increased TNFR expression correlated with an increase in TNF-induced superoxide production. In contrast, the 3 fatty acids eicosapentaenoic acid, docosahexaenoic acid, and linolenic acid failed to stimulate TNFR expression. Although fMLP and LPS reduced the neutrophil expression of TNFR, when pretreated with AA, fMLP caused an increase in TNFR expression. Consistent with this result was the finding that AA prevented the fMLP-induced receptor release in neutrophil cultures. AA also caused an increase in TNFR expression in matured HL-60 cells (neutrophil-like cells), but a decrease in nonmatured cells and HUVEC. The AA effects were independent of the lipoxygenase and cyclooxygenase pathways, but dependent on protein kinase C, the extracellular signal-regulated kinases 1 and 2, and cytosolic phospholipase A2. The data demonstrate a unique effect of AA in the inflammatory reaction, through its action on neutrophil TNFR expression, and suggest that AA may regulate the response of neutrophils to TNF by altering its receptor number. |
Keywords: | Endothelium, Vascular Neutrophils Cell Line HL-60 Cells Humans Superoxides Lipid Peroxides Phospholipases A Isoenzymes Lipoxygenase Mitogen-Activated Protein Kinases Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Protein Kinase C Lipopolysaccharides Fatty Acids, Unsaturated Arachidonic Acid Hydroxyeicosatetraenoic Acids Leukotrienes N-Formylmethionine Leucyl-Phenylalanine Receptors, Tumor Necrosis Factor Neutrophil Activation Down-Regulation Up-Regulation Prostaglandin-Endoperoxide Synthases Phospholipases A2 |
Rights: | Copyright © 2003 by The American Association of Immunologists |
DOI: | 10.4049/jimmunol.171.5.2616 |
Published version: | http://dx.doi.org/10.4049/jimmunol.171.5.2616 |
Appears in Collections: | Aurora harvest 5 Paediatrics publications |
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