Estrogen receptor‐α deficiency promotes increased TNF‐α secretion and bacterial killing by murine macrophages in response to microbial stimuli in vitro

摘要: In this series of studies, we determined the potential role intracellular estrogen receptors (ER), ERalpha and ERbeta, on macrophage function in response to bacterial stimuli. The sex hormone 17beta-estradiol (E(2)) ER have been shown modulate inflammatory responses as well T helper cell type 1 (TH1)/TH2 responses. mechanisms E(2) its use alter these immune functions remain largely unknown. ERbeta possess complex actions tissues where they are expressed. We characterized receptor repertoire murine dendritic cells thioglycollate-elicited peritoneal macrophages (PM). Both types express mRNA for ERalpha. Neither expressed detectable amounts mRNA, by reverse transcriptase-polymerase chain reaction using exon-specific primers spanning each seven intron/exon junctions. Primary from ERalpha- ERbeta-deficient severe combined immunodeficiency mice [ERalpha knockout (KO) ERssKO, respectively] were used delineate effects via which steroid function. ERalpha-deficient PM exposed ex vivo lipopolysaccharide or Mycobacterium avium exhibited significant increases tumor necrosis factor alpha (TNF-alpha) secretion reduction load when compared with wild-type (WT) PM. contrast, possessed no difference TNF-alpha WT littermates. These studies suggest that ERalpha, but not modulates