Monocyte chemotactic protein-1 in cervical and amniotic fluid: Relationship to microbial invasion of the amniotic cavity, intra-amniotic inflammation, and preterm delivery Bo Jacobsson, MD, PhD, a Rose-Marie Holst, MD, a Ulla-Britt Wennerholm, MD, PhD, a Bengt Andersson, MD, PhD, b Ha ˚kan Lilja, MD, PhD, a and Henrik Hagberg, MD, PhD a Go ¨teborg, Sweden OBJECTIVE: The purpose of this study was to evaluate the role of monocyte chemotactic protein-1 in cervical and amniotic fluid in women in preterm labor and with preterm premature rupture of membranes. STUDY DESIGN: Women with singleton pregnancies (#34 weeks) in preterm labor (n = 75 women), with preterm premature rupture of membranes (n = 47 women), and at term (n = 45 women) who were undergoing elective cesarean delivery were included. Cervical and amniotic fluid were sampled. RESULTS: Monocyte chemotactic protein-1 in cervical and amniotic fluid was higher in women in preterm labor than in women at term. Cervical monocyte chemotactic protein-1 in women in preterm labor was associated with microbial invasion of the amniotic cavity, intra-amniotic inflammation, delivery within 7 days, and at #34 weeks. Amniotic monocyte chemotactic protein-1 correlated to microbial invasion of the amniotic cavity in women with preterm premature rupture of membranes, intra-amniotic inflammation in preterm labor, preterm premature rupture of membranes, delivery within 7 days, and delivery at #34 weeks in women in preterm labor. CONCLUSION: Monocyte chemotactic protein-1 in cervical and amniotic fluid levels are elevated in preterm labor and preterm premature rupture of membranes and correlate to intra-amniotic infection/inflammation. (Am J Obstet Gynecol 2003;189:1161-7.) Key words: Monocyte chemotactic protein-1, amniotic fluid, cervical fluid, preterm birth Some normal functions of the female reproductive tract (such as parturition and cervical ripening) depend on inflammatory processes. 1 In addition, inflammation appears to be critical in certain pathologic processes (eg, in the preterm labor syndrome). 2 Modern understanding of reproductive functioning indicates the existence of local paracrine-autocrine regulatory mechanisms. 1 Inflammatory processes are regulated by a coordinated expression of proinflammatory and anti-inflammatory cytokines and chemokines. Chemokines (short for che- moattractant cytokines) play a crucial role in this process by regulating the leukocyte traffic. A great deal of research has identified the chemoattractants and activators that are responsible for neutrophil and lymphocyte traffic but less is known about the molecules that regulate monocyte migration. Certain chemokines, such as monocyte che- motactic protein-1 (MCP-1), have been demonstrated to recruit monocytes into foci of active inflammation. 3 MCP- 1 is considered to be a prototypic b-chemokine. It has been proved that MCP-1 is involved in several aspects of uterine function and in the local regulation of endometrial processes such as menstruation and implantation. 1 The preterm labor syndrome has been characterized as an inflammatory-like condition. 2 Several cytokines with proinflammatory properties (such as interleukin [IL]-6, IL-1b, IL-18, and tumor necrosis factor-a) are known to be involved in this process. 2 Information on chemokines in pregnancy has focused on IL-8, macrophage inflamma- tory protein (MIP)-1a, growth-related oncogene-a, and RANTES (regulated on activation, T-cell expressed and secreted). 4-7 RANTES and MIP-1a are other b-chemo- kines that have been studied in relation to preterm birth and proved to be increased in patients with microbial invasion of the amniotic cavity (MIAC). 4,6 Because of its critical role in the traffic of important cells in inflammatory processes and the host defense, MCP-1 might participate in providing a cervical/decid- ual defense line against MIAC and conceivably might serve as a cervical marker for MIAC and intra-amniotic From the a Department of Obstetrics and Gynecology, Perinatal Center, Institute for the Health of Women and Children, Go ¨teborg, Sweden, and the b Department of Clinical Immunology, Institute of Laboratory Medicine Sahlgrenska University Hospital, Go ¨teborg, Sweden. Supported by the Swedish Medical Research Council (09455), the Go ¨teborg Medical Society, and the Frimurare Barnhus Foundation and by Swedish government grants to researchers in public health service (ALF). Received for publication January 4, 2003; revised March 5, 2003; accepted May 1, 2003. Reprints not available from the authors. Corresponding author: Bo Jacobsson, MD, PhD, Department of Obstetrics and Gynecology, Sahlgrenska University Hospital/East, SE-416 85 Go ¨teborg, Sweden. E-mail: bo.jacobsson@obgyn.gu.se. Ó 2003, Mosby, Inc. All rights reserved. 0002-9378/2003 $30.00 + 0 doi:10.1067/S0002-9378(03)00594-5 1161