Model for biochemical cascades involved with preterm labor. Toll-like receptors recognize conserved bacterial motifs or proteins that are indicative of cellular damage to increase the production of arrays of proinflammatory cytokines that may differ between TLRs. These cytokines and chemokines can increase one another to augment their production, recruit neutrophils (NΦ) and macrophages (MΦ) to the maternal-fetal interfaces, and increase the production of downstream mediators of inflammation- the most important of which seem to be prostaglandins and matrix metalloproteinases. These downstream mediators have varying effects in different tissues. In the myometrium, prostaglandins contribute to increased uterine contractions and matrix metalloproteinases may contribute to detachment of the placenta. In the cervix, these mediators cause degradation of the extracellular matrix resulting in effacement and dilation. Increased activity of matrix metalloproteinases in the membranes reduces the pressure required for membrane rupture. During much of pregnancy, immunosuppressive substances such as progesterone (P4) and IL-10 suppress these proinflammatory cascades and downstream regulators such as the TIMPs and PGDH may also play a role in prolonging pregnancy. Current literature suggests that excessive levels of stress proteins or infectious organisms may override the protective effects of such molecules to cause preterm labor and/or PPROM.