Wen F Q, Watanabe K, Yoshida M
Second Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
Prostaglandins. 1996 Aug;52(2):93-102. doi: 10.1016/0090-6980(96)00055-x.
We evaluated the effect of interleukin-6 (IL-6) on the production of prostacyclin (PGI2) by cultured human pulmonary artery smooth muscle cells (HPASMC). Incubation of these cells for up to 48 h with IL-6 led to a dose- and time-dependent decrease in the concentration of PGI2 in the culture medium. The incubation of HPASMC with 10 micrograms/ml of lipopolysaccharide (LPS), 200 U/ml of IL-1 beta, or 500 U/ml of TNF alpha for 24 hr significantly increased the concentration of PGI2 in the medium. However, the addition of IL-6 to a medium containing LPS, IL-1 beta, or TNF alpha significantly inhibited the stimulatory effect of those substances on PGI2 production. Such inhibition was closely related to the concentration of IL-6. IL-6 may counteract the roles of LPS and of other cytokines on the regulation of pulmonary vascular tension in endotoxin- and cytokine-mediated disorders such as sepsis and the acute respiratory distress syndrome (ARDS).
我们评估了白细胞介素-6（IL-6）对培养的人肺动脉平滑肌细胞（HPASMC）前列环素（PGI2）生成的影响。用IL-6孵育这些细胞长达48小时导致培养基中PGI2浓度呈剂量和时间依赖性降低。用10微克/毫升脂多糖（LPS）、200单位/毫升IL-1β或500单位/毫升TNFα孵育HPASMC 24小时可显著增加培养基中PGI2的浓度。然而，向含有LPS、IL-1β或TNFα的培养基中添加IL-6可显著抑制这些物质对PGI2生成的刺激作用。这种抑制与IL-6的浓度密切相关。IL-6可能在内毒素和细胞因子介导的疾病如败血症和急性呼吸窘迫综合征（ARDS）中抵消LPS和其他细胞因子对肺血管张力调节的作用。
