Spontaneous labour at term is associated with fetal monocyte activation.
The aetiology of both term and preterm labour remains incompletely understood. Maternal infectious diseases as well as intra-uterine infections were shown to be a well established cause of uncontrollable preterm delivery, indicating that inflammatory reactions, regulated by maternal immunecompetent cells, are implicated in labour-promoting mechanisms. To investigate the possibility that the activation of the fetal immune system may be involved in labour induction, we examined cytokine production patterns of different cord blood cell populations obtained from neonates after spontaneous onset of normal term labour and vaginal delivery (n = 25), vaginal delivery but induced term labour (n = 17), and preterm delivery because of uncontrollable labour (n = 27, 20 patients received corticoid treatment for fetal lung maturation), in comparison with cells obtained from neonates after elective term caesarean delivery in the absence of labour (n = 15). Our results demonstrate that spontaneous term labour, but not induced term labour, was associated with significantly increased IL-6 production by myelomonocytic cell populations. Preterm delivery due to uncontrollable labour with resistance to tocolysis was not associated with increased IL-6 production by fetal myelomonocytic cells. Two-colour flow cytometry combined with intracellular cytokine staining was used to identify fetal monocytes as sources of labour-associated IL-6 release at term. We did not find any activation of cord blood T cells in association with spontaneous term or uncontrollable preterm labour. Therefore, fetal T cell responses may not cause monocyte activation. Our results suggest that increased release of IL-6 from fetal monocytes is involved in mechanisms promoting normal term, but not preterm labour, and that mechanisms inducing term and preterm labour are completely different.
Steinborn
A
A
Department of Obstetrics and Gynaecology, J.-W. Goethe-University of Frankfurt, Germany. Steinborn@em.uni-frankfurt.de
Sohn
C
C
Sayehli
C
C
Baudendistel
A
A
Hüwelmeier
D
D
Solbach
C
C
Schmitt
E
E
Kaufmann
M
M
D001623:Betamethasone / Q000627:therapeutic use; D002585:Cesarean Section; D036861:Delivery, Obstetric; D005260:Female; D005280:Fenoterol / Q000627:therapeutic use; D005312:Fetal Blood / Q000166:cytology* / Q000276:immunology; D005333:Fetus / Q000276:immunology* / Q000502:physiology; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D015850:Interleukin-6 / Q000096:biosynthesis / Q000378:metabolism*; D007751:Labor, Induced; D007743:Labor, Obstetric / Q000276:immunology* / Q000502:physiology; D008168:Lung / Q000196:embryology; D008278:Magnesium Sulfate / Q000627:therapeutic use; D009000:Monocytes / Q000378:metabolism / Q000502:physiology*; D007752:Obstetric Labor, Premature / Q000276:immunology / Q000503:physiopathology; D011247:Pregnancy; D015149:Tocolytic Agents / Q000627:therapeutic use
D015850:Interleukin-6; D015149:Tocolytic Agents; D005280:Fenoterol; D008278:Magnesium Sulfate; D001623:Betamethasone