Labour onset results from a complex interplay between hormonal and inflammatory signals. Untimely activation of these pathways can cause preterm labour (PTL) and premature birth (<37 weeks of gestation), the primary cause of infant mortality. Throughout gestation, uterine quiescence is maintained by progesterone and its withdrawal at term induces pro-labour genes and activation of uterine contractions. Infection and inflammation are frequently associated with PTL. Recognition of bacteria by the maternal innate immune system involves activation...