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.