{"title":"Inhibitory effect of interferon-alpha on respiratory burst and glucose metabolism in phagocytic cells.","authors":"M Conde, J Andrade, F J Bedoya, F Sobrino","doi":"10.1089/jir.1994.14.11","DOIUrl":null,"url":null,"abstract":"<p><p>Anion superoxide (O2-) production and glucose metabolism was studied in murine macrophages following in vivo or in vitro treatment with human recombinant interferon-alpha 2b (IFN-alpha 2b). The PMA-dependent O2- production was inhibited by IFN-alpha 2b in a concentration- and time-dependent manner. NO2- production by macrophages in culture was slightly inhibited (about 16%) at 30 nM IFN-alpha and a clear decrease (35%) was obtained with 150 nM IFN-alpha. Low doses (0.3 and 3 nM IFN-alpha) had no effect. Also, IFN-alpha 2b inhibited lactate release and 3H2O production from [2-3H] and [3-3H]glucose in macrophages isolated after in vivo treatment for 24 h. The data support an inhibitory role of IFN-alpha in the metabolic activation of macrophages and suggest a putative mechanism for the inhibition of some macrophage functions as previously reported.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 1","pages":"11-6"},"PeriodicalIF":0.0000,"publicationDate":"1994-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.11","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of interferon research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/jir.1994.14.11","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
Anion superoxide (O2-) production and glucose metabolism was studied in murine macrophages following in vivo or in vitro treatment with human recombinant interferon-alpha 2b (IFN-alpha 2b). The PMA-dependent O2- production was inhibited by IFN-alpha 2b in a concentration- and time-dependent manner. NO2- production by macrophages in culture was slightly inhibited (about 16%) at 30 nM IFN-alpha and a clear decrease (35%) was obtained with 150 nM IFN-alpha. Low doses (0.3 and 3 nM IFN-alpha) had no effect. Also, IFN-alpha 2b inhibited lactate release and 3H2O production from [2-3H] and [3-3H]glucose in macrophages isolated after in vivo treatment for 24 h. The data support an inhibitory role of IFN-alpha in the metabolic activation of macrophages and suggest a putative mechanism for the inhibition of some macrophage functions as previously reported.