Bisphenol　A　(BPA)　is　a　well-known　environmental　endocrine-disrupting　chemical.　Employing　primary　macrophages　from　head　kidney　of　red　common　carp　(Cyprinus　carpio),　the　present　study　aimed　to　evaluate　the　immune　modulatory　effect　of　BPA　and　to　explore　its　potential　action　mechanism　associated　with　estrogen　receptor　(ER)　and　nuclear　factor-kappa　B　(NF-kappa　B)　pathways.　A　dynamic　response　process　was　observed　in　macrophages　upon　various　concentrations　of　BPA　exposure,　which　significantly　enhanced　the　antibacterial　activity　of　macrophages　at　0.1,　1,　or　10　mu　g/L,　but　instead　induced　the　apoptosis　at　100,　1000,　and　10　000　mu　g/L.　A　potential　pro-inflammatory　effect　of　BPA　exposure　was　suggested,　judging　from　the　increased　production　of　nitrite　oxide　and　reactive　oxygen　species　(ROS),　the　induction　of　interleukin-1　beta　mRNA　and　protein,　as　well　as　NF-kappa　B　and　other　NF-kappa　B-associated　immune　gene　expression.　Following　BPA　coexposure　with　the　ER　or　NF-kappa　B　antagonist,　the　induction　of　ROS,　ERa,　and　NF-kappa　B-associated　immune　gene　expression　was　significantly　inhibited,　implying　interaction　between　those　two　pathways.　This　study　thus　indicated　that　low　doses　of　BPA　exposure　alone　could　significantly　disturb　the　immune　response　of　fish　primary　macrophages　in　vitro,　and　for　the　first　time　revealed　the　synergistic　action　of　ERa　and　NF-kappa　B　transcription　factors　in　the　BPA　effect.