Abstract
The precise mechanisms for the onset of labor at term remain unknown, yet several studies in humans reveal the role of cytokines in the initiation and maintenance of labor, showing many of the hallmarks of inflammation. Recent findings suggest a possible relationship between the activity of the autonomic nervous system (ANS) and the vagal anti-inflammatory response during labor. Furthermore, the role of vaginal microbiota is particularly important during pregnancy because vaginal dismicrobism is one of the most important mechanisms associated with preterm birth. In this review, we present evidence suggesting that a sterile anti-inflammatory response is manifested to attenuate the excessive inflammation introduced by low-risk labor at term, involving either the action of a cholinergic pathway, uterine-like myokines or the vaginal microbiome.