This paper reviews the mechanisms leading to the commencement of labor in the presence of intrauterine infection. It is postulated that induction of preterm contractions represents an escape mechanism of the fetus from a hostile environment. Bacterial toxins provoke an immunological response (macrophages) of the fetomaternal compartment. Liberation of cytokines (IL-1, IL-6, IL-8) stimulates prostanoid synthesis in the decidua and amnion, as well as migration of granulocytes into the cervix. Additional still unknown factors may determine whether this process leads to cervical dilatation, effacement and finally preterm delivery. The role is discussed of other cytokines, i.e., colony-stimulating factors, transforming growth factor beta, and interleukin receptor antagonists as potential, clinically useful tocolytics in this labile equilibrium.