Continues to be a major public health issue and the number one cause of neonatal death. Among the important events contributing to labor is the ripening/ remodeling of the cervix. Changes in the cervical structure soften and dilate the cervix allowing the passage of the fetus forced by rhythmic myometrial contractions. We previously demonstrated that complement activation plays a crucial role in the cervical remodeling Angoroside-C process that leads to preterm labor. Using a mouse model of PTD induced by LPS we found that complement split product C5a attracts and activates macrophages to the cervix. In response C5a, macrophages release metalloproteinases that degrade collagen, increasing the cervix distensibility and leading to PTD in mice. The aim of this study is to characterize the term cervical ripening process and compare it with preterm. Knowing that complement activation plays a causative role in PTD in mice, we decided to study if complement activation also plays a role in cervical remodeling at term. If complement activation is not involved in the physiological process that leads to term delivery we will then have identified a Escitalopram Oxalate possible specific and selective target to prevent PTD and thus improve neonatal health. Is cervical remodeling in PTD caused by the same mechanism/s that cause/s cervical remodeling at term but these changes are accelerated in time? This question has been pondered by obstetricians seeking for strategies to prevent PTD for many years. To answer this question we investigated the initiators and cellular effectors in a mouse model of preterm delivery and in control mice that delivered at term. We previously described that complement activation plays a causative role in PTD in mice. Thus, we sought to investigate if complement activation also plays a role in cervical remodeling at term. Here we found that complement activation is not involved in the physiological process that leads to term delivery suggesting that we identified a possible specific and selective target to prevent PTD. In addition, serum complement C3a and C5a levels, that increased during PTD did not increase in mice that deliver at term. That C3a and C5a increase only during PTD suggests that they can be potential biomarkers. This is in agreement with several clinical studies that demonstrate a potential role of complement split products as biomarkers of PTD. Recent studies in mice suggested that the mechanisms of cervical remodeling in preterm birth is different from normal ripening at term. In one of these studies the expression of proinflammatory genes is upregulated in preterm birth compared to term. The other study demonstrated that cervical ripening preterm can be initiated by more than one mechanism and it is not necessarily an acceleration of the physiological process at term. Our data suggest that the cervical ripening at term is a process non-leukocyte dependent.