Dixon CL, et al. - Researchers performed this study to investigate p38MAPK activation-induced fetal membrane cell senescence in response to inflammation (tumour necrosis factor-alpha [TNF-α]) and infection (lipopolysaccharide [LPS]), factors associated with spontaneous preterm birth. In this study, OS-mediated p38MAPK induction, senescence, and IL-6 increase from amnion epithelial cells (AECs) were shown to be caused by TNF-α. Furthermore, it was noted that senescence and IL-6 increase were also induced by LPS. In addition, inflammatory and infectious factors may cause premature fetal cell senescence contributing to preterm birth pathophysiology.