caa a22 4500 465765556 CHVBK 20180323111912.0 cr unu---uuuuu 170327e19900601xx s 000 0 eng 10.1007/BF02544341 doi (NATIONALLICENCE)springer-10.1007/BF02544341 Arachidonic acid regulates the binding of human interferon in human skin fibroblasts [Elektronische Daten] [Sree Menon, W. Yap, Andrew Lim, Y. Tan] The induction of the antiviral state in human fibroblasts by human interferon is inhibited by arachidonic acid, its analogues 5,8,11,14-eicosatetraynoic and 5,8,11-eicosatriynoic acids, as well as by sodium arachidonate. The fatty acids myristic or oleic acid and sodium palmitate do not inhibit the antiviral action of interferon. Experiments were conducted to investigate the mechanism by which arachidonic acid could inhibit the action of interferon. No correlation between cellular lipoxygenase activities and the inhibition of antiviral action of interferon was observed in the fatty acid treated cells. Likewise, the cyclooxygenase inhibitors indomethacin and oxyphenylbutazone do not inhibit the interferon-induced antiviral state. Taken together, the inhibition of interferon action by arachidonates is unlikely to be mediated by cyclooxygenase or lipoxygenase-generated intermediates, even though arachidonates are known to affect the activity of these enzymesin vitro. Measurement of interferon receptors in the fatty acid treated cells showed that arachidonic acid sodium arachidonate and its analogues decreased the number of human type I interferon receptors available for binding, and inhibited the transcription of the interferon-induced 6-16 gene and the induction of cellular (2′-5′)-oligoadenylate synthetase, suggesting the mechanism of inhibition is mediated at the level of the interferon receptor. The significance of the finding that arachidonic acid, a common fatty acid of cells and serum, can affect the antiviral action of interferon is discussed. American Oil Chemists' Society, 1990 Menon Sree Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut Yap W. Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut Lim Andrew Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut Tan Y. Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut Lipids Springer-Verlag 25/6(1990-06-01), 321-327 0024-4201 25:6<321 1990 25 11745 https://doi.org/10.1007/BF02544341 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02544341 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Menon Sree Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut NATIONALLICENCE 700 1- Yap W. Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut NATIONALLICENCE 700 1- Lim Andrew Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut NATIONALLICENCE 700 1- Tan Y. Institute of Molecular and Cell Biology, National University of Singapore, 10 Kent Ridge Crescent, 05121, Singapore, Singapore aut NATIONALLICENCE 773 0- Lipids Springer-Verlag 25/6(1990-06-01), 321-327 0024-4201 25:6<321 1990 25 11745 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer