title: Estrogen, but not testosterone, down-regulates cytokine production in nicotine-induced murine macrophage.
abstract: We have investigated the effects of 17beta-estradiol (E2) and testosterone (Te) on the production of proinflammatory factors by nicotine-induced murine macrophage (Ana-1). Ana-1 pretreated with or without E2/Te was challenged with different doses of nicotine at various time points. TNF-alpha, IL-1beta IFN-gamma, and IL-8 in the supernatant of Ana-1 were detected using radioimmunoassay (RIA) or enzyme-linked immunosorbent assay (ELISA). The presence of estrogen and androgen receptors in Ana-1 was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. E2 could obviously suppress the expression of TNF-alpha and IL-1beta whereas Te could not. There were no obvious changes in the levels of either IL-8 or IFN-gamma in Ana-1 stimulated with nicotine or sex hormones (p>0.05). The antagonist tamoxifen of E2 abolished the effects of E2 on TNF-alpha and IL-1beta whereas the antagonist cyproterone of Te did not alter the effects of Te on Ana-1. Furthermore, RT-PCR and Western blotting showed that both the estrogen receptors (ER-alpha and ER-beta existed in Ana-1; however, androgen receptor (AR) was not detectable. Our data suggested that E2 could regulate the immunoreaction in the nicotine-induced inflammatory process possibly through classic intercellular ER, whereas Te had no significant effect in this process.
authors.affiliation: School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Zhao
authors.forename: Z
authors.initials: Z
authors.lastname: Qiao
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D015536:Down-Regulation / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D011944:Receptors, Androgen / Q000096:biosynthesis / Q000378:metabolism; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013739:Testosterone / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D004967:Estrogens; D018722:Nicotinic Agonists; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D014409:Tumor Necrosis Factor-alpha; D013739:Testosterone; D004958:Estradiol; D012313:RNA; D009538:Nicotine