Divers M J, Miller D, Bulmer J N, Vail A, Lilford R J
Dept of Obstetrics and Gynaecology, Royal Infirmary of Edinburgh, Scotland, UK.
Eur J Obstet Gynecol Reprod Biol. 1995 Oct;62(2):209-12. doi: 10.1016/0301-2115(95)02200-q.
To search for evidence of immune activation in idiopathic preterm term labour by measuring the soluble markers of T cell activation, CD8 (sCD8) and interleukin-2 receptor (sIL2R).
Serum sCD8 and sIL-2R were measured by commercial ELISA in subjects undergoing idiopathic preterm labour (PTL; n = 15) and normal term labour (TL; n = 17). Two gestationally equivalent non-labouring groups were also included representing preterm (PTC; n = 10) and term (TC; n = 10) controls. Possible delayed responses in soluble activation markers were monitored in blood samples taken 48 h after delivery in both labouring groups (PTLp; n = 9: TLp; n = 9).
(1) Excluding the 48 h postpartum samples, no statistically significant differences were revealed following a Kruskall-Wallis analysis of variance (ANOVA) for levels of sIL-2R (P = 0.093) and sCD8 (P = 0.098). Including the postpartum samples, however, gave statistically significant differences for each (sIL-2R: P = 0.033; sCD8: P = 0.006). (2) No statistically significant difference was revealed by direct comparison of the two labouring groups alone (Wilcoxon-Mann-Whitney test: P > 0.05). (3) Significantly lower levels of sCD8 were found in the PTL subgroup which had histological evidence of inflammation (Wilcoxon-Mann-Whitney: P = 0.003).
Statistical analysis of our data suggests that idiopathic preterm labour is not commonly associated with significant elevations in circulating sCD8 or sIL-2R levels compared with normal term labour. Where significant changes in the levels of these markers do arise, our evidence points to a delayed effect of labour per se rather than infection as the most probable cause.
通过测量T细胞活化的可溶性标志物CD8(可溶性CD8,sCD8)和白细胞介素-2受体(可溶性白细胞介素-2受体,sIL2R),寻找特发性早产分娩中免疫激活的证据。
采用商业酶联免疫吸附测定法(ELISA)检测特发性早产(PTL;n = 15)和足月正常分娩(TL;n = 17)受试者血清中的sCD8和sIL - 2R。还纳入了两个孕周相当的未分娩组,分别代表早产(PTC;n = 10)和足月(TC;n = 10)对照。在两个分娩组(PTLp;n = 9:TLp;n = 9)产后48小时采集的血样中监测可溶性活化标志物可能的延迟反应。
(1)排除产后48小时的样本,对sIL - 2R水平(P = 0.093)和sCD8水平(P = 0.098)进行克鲁斯卡尔 - 沃利斯方差分析(ANOVA)后,未发现统计学上的显著差异。然而,纳入产后样本后,每项均出现统计学上的显著差异(sIL - 2R:P = 0.033;sCD8:P = 0.006)。(2)仅对两个分娩组进行直接比较,未发现统计学上的显著差异(威尔科克森 - 曼 - 惠特尼检验:P > 0.05)。(3)在有组织学炎症证据的PTL亚组中,sCD8水平显著较低(威尔科克森 - 曼 - 惠特尼检验:P = 0.003)。
对我们数据的统计分析表明,与足月正常分娩相比,特发性早产通常与循环sCD8或sIL - 2R水平的显著升高无关。当这些标志物水平确实出现显著变化时,我们的证据表明分娩本身的延迟效应而非感染是最可能的原因。