The etiology of PTB is complex and multifactorial. Key mechanisms leading to PTB include the early activation of the fetal hypothalamic–pituitary–adrenal axis in response to maternal and/or fetal stress, premature placental abruption, uterine expansion problems, cervical insufficiency and inflammation, especially in the urogenital tract [5]. Preterm prelabor rupture of the membranes (PPROM) also contributes to a high incidence of PTB. PPROM is mainly triggered by inflammation associated with an infection, where inflammatory cytokines weaken the fetal membranes [6–9].