Abstract
Prolonged labor, a major obstetric complication, is often linked to inadequate cervical ripening, which hinders labor progression. The process of cervical ripening is governed by complex hormonal and immune-mediated mechanisms, with monocytes playing a central role. These immune cells infiltrate the cervix and differentiate into macrophages, releasing cytokines and proteases that are essential for extracellular matrix (ECM) remodeling, cervical softening, and dilation. However, in prolonged labor, an imbalance in monocyte activity may impede normal cervical ripening, contributing to stalled labor and increased risk of maternal and neonatal complications. Monocytes are critical to the inflammatory response that initiates cervical remodeling during labor. Upon recruitment to the cervix, monocytes release inflammatory cytokines like interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha, which activate matrix metalloproteinases to degrade collagen and ECM proteins, facilitating cervical effacement and dilation. Dysregulated monocyte recruitment and prolonged inflammation, however, may lead to ineffective cervix remodeling, preventing labor from progressing efficiently. Furthermore, these immune responses can influence uterine contractility, either promoting or inhibiting uterine contractions, which further complicates the pathophysiology of prolonged labor.