Department of Surgery Saint Louis University School of Medicine Health Sciences Center 3635 Vista Avenue at Grand Boulevard St Louis Missouri 63110-0250 USA.
Mediators Inflamm. 1996;5(6):449-52. doi: 10.1155/S0962935196000622.
We investigated whether an interleukin 1 receptor antagonist (IL-1ra) altered cellular release of prostanoids and leukotrienes in a transformed colonic cell line (CACO-2) in the presence of proinflammatory stimuli. Cellular inflammation was induced by treatment with lipopolysaccharide (LPS) or the cytokine, interleukin 1 beta (IL-1(beta)). In a separate set of experiments, cells were pretreated with IL-1ra prior to exposure to LPS or IL-1(beta). Prostaglandin E(2) and leukotriene B(4) (LTB(4)) levels were quantified by ELISA assays. Both LPS and IL-1(beta) exposure were noted to stimulate cellular PGE(2) release, a response which was significantly inhibited by IL-1ra treatment. Either stimulant when administered alone failed to stimulate release of LTB(4). When administered after IL-1ra pretreatment however, both stimuli caused a significant increase in LTB(4) release. These results suggest that a cytokine receptor antagonist can selectively influence eicosanoid production in this cell line. Furthermore, this study suggests that a IL-1ra may have a future clinical role in the treatment of inflammatory disorders of the colon which are intimately linked to enhanced eicosanoid synthesis.
我们研究了白细胞介素 1 受体拮抗剂 (IL-1ra) 是否会改变存在促炎刺激物的情况下转化结肠细胞系 (CACO-2) 中前列腺素和白三烯的细胞释放。通过用脂多糖 (LPS) 或细胞因子白细胞介素 1β (IL-1β) 处理诱导细胞炎症。在一组单独的实验中，细胞在用 LPS 或 IL-1β 暴露之前用 IL-1ra 预处理。通过 ELISA 测定法定量测定前列腺素 E2 (PGE2) 和白三烯 B4 (LTB4) 水平。LPS 和 IL-1β 暴露都被观察到刺激细胞 PGE2 释放，IL-1ra 处理显著抑制了这种反应。单独给予任何一种刺激剂均未能刺激 LTB4 的释放。然而，当在用 IL-1ra 预处理后给予时，两种刺激剂均导致 LTB4 释放显著增加。这些结果表明，细胞因子受体拮抗剂可以选择性地影响该细胞系中类二十烷酸的产生。此外，这项研究表明，IL-1ra 可能在治疗与增强的类二十烷酸合成密切相关的结肠炎症性疾病方面具有未来的临床作用。
