Cytokines and preterm labour

Preterm labour and its consequences are the major contributors to perinatal morbidity and mortality worldwide. The prevention of preterm labour and delivery is the single most important challenge to modern obstetrics today. Progress in this area has been hampered by lack of understanding of the basic mechanisms responsible for preterm labour. The implicit paradigm which has governed the study of parturition, is that term and preterm labour are fundamentally the same processes except for the gestational age at which they occur. Indeed, they share a common terminal pathway composed of uterine contractility, cervical dilatation and rupture of membranes. We proposed that while term labour is the result of physiological activation of this common terminal pathway, preterm labour and delivery is the consequence of pathological activation.1Thus, preterm labour may be considered as the response of the fetomaternal unit to a variety of insults (e.g. chorioamnionitis, ischaemia, fetal growth restriction, etc.) (Fig 1) If these insults cannot be effectively handled in the context of a continuing pregnancy, then labour and delivery may occur.