The aetiology of both term and preterm labour remains incompletely understo
od. Maternal infectious diseases as well as intra-uterine infections were s
hown to be a well established cause of uncontrollable preterm delivery, ind
icating that inflammatory reactions, regulated by maternal immunecompetent
cells, are implicated in labour-promoting mechanisms. To investigate the po
ssibility that the activation of the fetal immune system may be involved in
labour induction, we examined cytokine production patterns of different co
rd blood cell populations obtained from neonates after spontaneous onset of
normal term labour and vaginal delivery (n = 25), vaginal delivery but ind
uced term labour (n = 17), and preterm delivery because of uncontrollable l
abour (n = 27, 20 patients received corticoid treatment for fetal lung matu
ration), in comparison with cells obtained from neonates after elective ter
m caesarean delivery in the absence of labour (n = 15). Our results demonst
rate that spontaneous term labour, but not induced term labour, was associa
ted with significantly increased IL-6 production by myelomonocytic cell pop
ulations. Preterm delivery due to uncontrollable labour with resistance to
tocolysis was not associated with increased IL-6 production by fetal myelom
onocytic cells. Two-colour flow cytometry combined with intracellular cytok
ine staining was used to identify fetal monocytes as sources of labour-asso
ciated IL-6 release at term. We did not find any activation of cord blood T
cells in association with spontaneous term or uncontrollable preterm labou
r. Therefore, fetal T cell responses may not cause monocyte activation. Our
results suggest that increased release of IL-6 from fetal monocytes is inv
olved in mechanisms promoting normal term, but not preterm labour, and that
mechanisms inducing term and preterm labour are completely different.