Spontaneous labour at term is associated with fetal monocyte activation

Citation
A. Steinborn et al., Spontaneous labour at term is associated with fetal monocyte activation, CLIN EXP IM, 117(1), 1999, pp. 147-152
Citations number
33
Categorie Soggetti
Immunology
Journal title
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
ISSN journal
00099104 → ACNP
Volume
117
Issue
1
Year of publication
1999
Pages
147 - 152
Database
ISI
SICI code
0009-9104(199907)117:1<147:SLATIA>2.0.ZU;2-7
Abstract
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.