In this context, an interesting observation is that pregnancies with preterm birth due to infection show significantly higher levels of CRH, urocortin 2, and CRH-R1 in comparison with patients with idiopathic preterm birth or premature rupture of membranes without infection (34), suggesting that placental expression of stress-related pathways is activated in infective processes. Here, CRHR1 is linked to spontaneous preterm birth.