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(American Journal of Pathology. 2006;169:967-976.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.050207

Disruption of Interleukin-18, but Not Interleukin-1, Increases Vulnerability to Preterm Delivery and Fetal Mortality after Intrauterine Inflammation

Xiaoyang Wang*{dagger}, Henrik Hagberg*{ddagger}, Carina Mallard*{ddagger}, Changlian Zhu*{dagger}, Maj Hedtjärn*, Carl-Fredrik Tiger§, Kristina Eriksson, Åsa Rosen{ddagger} and Bo Jacobsson{ddagger}||

From the Department of Physiology,* Perinatal Center, and the Departments of Microbiology§ and Rheumatology and Inflammation Research, Göteborg University, Göteborg, Sweden; the Department of Pediatrics,{dagger} the Department of Obstetrics and Gynecology,{ddagger} Perinatal Center, Sahlgrenska Academy, Göteborg, Sweden; The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China; and the North Atlantic Neuro-Epidemiology Alliances,|| University of Aarhus, Aarhus, Denmark

Preterm birth is a major contributor of adverse perinatal outcome. Clinical data suggest that an inflammatory response is important in the process leading to preterm labor. By using a recently introduced mouse model of localized intrauterine lipopolysaccharide-induced inflammation, the effect of interleukin (IL)-18 gene disruption and/or IL-18 neutralization as well as combined IL-1{alpha}/ß gene disruption on inflammation-induced fetal loss was investigated. The frequency of preterm fetal loss was significantly higher in IL-18 knockout mice (58.9%) and in mice administered IL-18-binding protein (59.7%) compared to wild-type controls (34.7%). The rate of fetal loss was not affected by IL-1{alpha}/ß gene deficiency (38.7%). Decreased IL-18 protein expression combined with elevated IL-12 protein expression in uterine tissue of IL-18 knockout mice and IL-18-binding protein-treated animals was noticed. These data demonstrate that preterm pregnancy loss in response to intrauterine inflammation was enhanced by disruption of the IL-18 gene and/or IL-18 neutralization, events that may relate to exaggerated Th1 responses because of an increased IL-12/IL-18 ratio.




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K. Skogstrand, D. M. Hougaard, D. E. Schendel, N.-P. Bent, C. Svaerke, and P. Thorsen
Association of Preterm Birth With Sustained Postnatal Inflammatory Response
Obstet. Gynecol., May 1, 2008; 111(5): 1118 - 1128.
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