Figure 1.

Indicators of inflammatory activation in fetal and maternal tissues during preterm labour. Inflammatory activation is central to parturition, with molecular and cellular changes that manifest in the fetal and maternal compartments. In maternal tissues including the myometrium, decidua and cervix, recruitment of inflammatory leucocytes and elevated expression of pro‐inflammatory cytokines and chemokines are evident. These pro‐inflammatory mediators upregulate uterine activation genes, in turn causing myometrial contractions and cervical effacement and dilation. Macrophages infiltrate the placenta and cause elevated production of pro‐inflammatory cytokines. The fetal membranes (amnion and chorion) express elevated inflammatory cytokines, which access uterine tissues to promote uterine activation gene expression and amplify MMP production, instigating fetal membrane rupture. In the amniotic fluid, elevated accumulation of inflammatory cytokines and chemokines may be transmitted to the fetal and maternal tissues. The underlying pro‐inflammatory drivers in preterm labour are a consequence of infection, or sterile tissue insult or injury.