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anis s o tly nt ch-in of chemokines like C-X-C motif ligand 3 (CXCL3) and extracellular matrix remodeling signaling molecules like tenascin C (TNC). Our data suggest that IL-1b elicits the rapid activation of a cellular network of genes particularly implicated in inflammatory response that neutrophils. The release of proinflammatory cytokines nancy and labor (Lappas et al. 2002). Under normal myometrial cell function. In particular, we were induces phospholipid metabolizing enzymes and theDOI: 10.1530/REP-07-0289release of prostaglandins (Zaragoza et al. 2006). It has q 2007 Society for Reproduction and Fertilityinterested in uncovering the early response of uterine smooth muscle cells to IL-1b exposure. First, wePreterm birth, defined as infants who are delivered before 37 weeks of gestation, accounts for 6–10 % of all births and is a major risk factor for infant morbidity and mortality (Slattery & Morrison 2002). Cervical and intrauterine infection and inflammation in the mother are present inw30–50 % of preterm labor cases (Gomez et al. 1997, Challis et al. 2002). Bacterial infection leads to the activation of macrophages and lymphocytes. The subsequent release of proinflammatory cytokines such as interleukin-1b (IL-1b), IL6, tumor necrosis factor a (TNFa), and the chemotactic protein IL8 attracts additional macrophages as well as eosinophils and conditions, elevated levels of IL-1b are observed in amniotic fluid only late in pregnancy. In contrast, upon infection, the levels of IL-1b, IL6, TNFa, and IL8 are significantly increased, possibly leading to the early onset of labor (Romero et al. 1989, Saji et al. 2000, Suzuki et al. 2006). Recent data in nonhuman primate and mouse models further support the notion that specifically IL-1b and TNFa play a pivotal role in triggering preterm labor (Hirsch et al. 2006, Sadowsky et al. 2006). In this study, we wanted to further explore the link between the presence of proinflammatory cytokines andmay create a cellular environment favorable for myometrial cell contraction. Our results provide novel insights into the mechanisms of uterine smooth muscle cell regulation and possibly infection-induced preterm labor