Abstract
Background: The mechanisms underlying the initiation of premature uterine contractions during pregnancy are not fully understood. It is now widely accepted that proinflammatory cytokines are key mediators of the inflammatory signaling pathways in term or preterm labor. However, the exact triggers for inflammation-induced labor remain to be identified.
Method: We review the published literature and summarize the possible pathophysiological mechanisms underlying the initiation of uterine contractions with a particular emphasis on intrauterine infection.
Result: Term and preterm labor are associated with inflammation-induced infiltration of leukocytes into the myometrium, cervix, decidua, and fetal membranes. During labor, peripheral leukocytes invade uterine tissues and secrete bactericidal mediators such as proinflammatory cytokines, resulting in initiation of uterine activity and labor. When these pathophysiological mechanisms occur too early in pregnancy, they may lead to preterm labor. The initiation of inflammatory cascades within the myometrium or intrauterine compartments must be tightly regulated to prevent premature activation of the inflammatory signals and to prevent premature uterine activation.
Conclusion: Labor in humans and rodents is associated with inflammation and the increased uterine contractions during labor are regulated by a complex of signaling pathways between pro-and antiinflammatory cytokines and between mother and fetus. Labor can be triggered from different sources including maternal, fetal and general infection. Therefore it is vital for pregnant women to avoid infection-related pathology and seek medical advice immediately to avoid premature uterine contractions or perhaps abortion.