Bry K, Lappalainen U
Department of Pediatrics, University of California, Irvine 92717.
Am J Obstet Gynecol. 1994 Apr;170(4):1194-8. doi: 10.1016/s0002-9378(94)70121-0.
Increased production of prostaglandins is associated with parturition. The production of interleukin-1 is increased in preterm labor occurring in the setting of infection. Interleukin-1 receptor antagonist prevents the effects of interleukin-1. Interleukin-4 and transforming growth factor-beta inhibit the production of prostaglandin E2 by monocytes and amnion cells, respectively. In addition, these cytokines enhance the production of interleukin-1 receptor antagonist by monocytes. We investigated whether the production of prostaglandin E2 and interleukin-1 receptor antagonist by decidual cells is modulated by interleukin-4 and transforming growth factor-beta 1.
Human decidual cells in monolayer culture were treated for 44 hours with interleukin-4 (1 to 100 ng/ml), transforming growth factor-beta 1 (1 to 10 ng/ml), the combination of these cytokines, or vehicle. Production of prostaglandin E2 and interleukin-1 receptor antagonist was measured by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. The Wilcoxon signed-rank test was used.
Both interleukin-4 and transforming growth factor-beta 1 inhibited prostaglandin E2 production by decidual cells (p < 0.01). Decidual cells produced interleukin-1 receptor antagonist at a basal rate of 26.4 +/- 6.7 pg/micrograms protein per 44 hours (n = 13). Interleukin-4 stimulated the production of interleukin-1 receptor antagonist by decidual cells (p < 0.01). Transforming growth factor-beta 1 potentiated the stimulatory effect of interleukin-4 on decidual cell interleukin-1 receptor antagonist production (p < 0.05).
By suppressing the production of prostaglandin E2 and enhancing the production of interleukin-1 receptor antagonist by decidual cells, interleukin-4 and transforming growth factor-beta may have a role in inhibiting preterm labor in the setting of infection.
前列腺素生成增加与分娩有关。在感染情况下发生的早产中，白细胞介素-1的生成会增加。白细胞介素-1受体拮抗剂可阻止白细胞介素-1的作用。白细胞介素-4和转化生长因子-β分别抑制单核细胞和羊膜细胞中前列腺素E2的生成。此外，这些细胞因子可增强单核细胞中白细胞介素-1受体拮抗剂的生成。我们研究了蜕膜细胞中前列腺素E2和白细胞介素-1受体拮抗剂的生成是否受白细胞介素-4和转化生长因子-β1的调节。
将单层培养的人蜕膜细胞用白细胞介素-4（1至100 ng/ml）、转化生长因子-β1（1至10 ng/ml）、这些细胞因子的组合或赋形剂处理44小时。分别通过放射免疫测定法和酶联免疫吸附测定法测量前列腺素E2和白细胞介素-1受体拮抗剂的生成。使用Wilcoxon符号秩检验。
白细胞介素-4和转化生长因子-β1均抑制蜕膜细胞中前列腺素E2的生成（p < 0.01）。蜕膜细胞以每44小时26.4±6.7 pg/μg蛋白质的基础速率产生白细胞介素-1受体拮抗剂（n = 13）。白细胞介素-4刺激蜕膜细胞产生白细胞介素-1受体拮抗剂（p < 0.01）。转化生长因子-β1增强了白细胞介素-4对蜕膜细胞白细胞介素-1受体拮抗剂生成的刺激作用（p < 0.05）。
通过抑制前列腺素E2的生成并增强蜕膜细胞中白细胞介素-1受体拮抗剂的生成，白细胞介素-4和转化生长因子-β可能在抑制感染情况下的早产中发挥作用。
