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Disruption of interleukin-18, but not interleukin-1, increases vulnerability to preterm delivery and fetal mortality after intrauterine inflammation

Journal article
Authors Xiaoyang Wang
Henrik Hagberg
Carina Mallard
Changlian Zhu
Maj Hedtjärn
Carl Fredrik Tiger
Kristina Eriksson
Åsa Rosen
Bo Jacobsson
Published in Am J Pathol
Volume 169
Issue 3
Pages 967-76
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Clinical Sciences
Pages 967-76
Language en
Keywords Animals, Female, Fetal Death/chemically induced/*genetics/immunology/pathology, Glycoproteins/immunology/pharmacology, Inflammation/chemically induced/genetics/immunology/pathology, Intercellular Signaling Peptides and Proteins, Interleukin-1/*deficiency/immunology, Interleukin-12/immunology, Interleukin-18/*genetics/immunology, Lipopolysaccharides/pharmacology/toxicity, Mice, Mice, Knockout, Pregnancy, Th1 Cells/immunology/pathology, Uterus/immunology/pathology
Subject categories Medical and Health Sciences, Internal medicine


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-1alpha/beta 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-1alpha/beta 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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