Masur H, Murray H W, Jones T C
Infect Immun. 1982 Feb;35(2):709-14. doi: 10.1128/iai.35.2.709-714.1982.
To define the suppressive effects of corticosteroids on mononuclear phagocyte antiprotozoal activity, normal resident peritoneal macrophages were exposed to hydrocortisone (HC) before, during, and after in vitro activation with cell-free supernatants (lymphokines). The presence of pharmacological concentrations of HC before or during lymphokine activation prevented normal macrophages from acquiring the capacity to either respond oxidatively to Toxoplasma gondii ingestion or to inhibit intracellular toxoplasma replication. HC had no effect, however, on the cells fully stimulated by lymphokine or on macrophages previously activated in vivo. These findings indicate that although HC does not impair the ability of activated macrophages to control intracellular protozoan infection, it does compromise the antimicrobial activity of the cell-mediated immune system by rendering normal macrophages unresponsive to lymphokine.
为了确定皮质类固醇对单核吞噬细胞抗原生动物活性的抑制作用,在体外用无细胞上清液(淋巴因子)激活正常的常驻腹膜巨噬细胞之前、期间和之后,将其暴露于氢化可的松(HC)。在淋巴因子激活之前或期间存在药理浓度的HC会阻止正常巨噬细胞获得对摄入弓形虫产生氧化反应或抑制细胞内弓形虫复制的能力。然而,HC对被淋巴因子完全刺激的细胞或先前在体内被激活的巨噬细胞没有影响。这些发现表明,虽然HC不会损害活化巨噬细胞控制细胞内原生动物感染的能力,但它确实会通过使正常巨噬细胞对淋巴因子无反应而损害细胞介导免疫系统的抗菌活性。