Description
Preterm birth is an important unsolved clinical problem.  Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities.  In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment.  Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions.  Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.