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

Artikel i vetenskaplig tidskrift
Författare Xiaoyang Wang
Henrik Hagberg
Carina Mallard
Changlian Zhu
Maj Hedtjärn
Carl Fredrik Tiger
Kristina Eriksson
Åsa Rosen
Bo Jacobsson
Publicerad i Am J Pathol
Volym 169
Nummer/häfte 3
Sidor 967-76
Publiceringsår 2006
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för kliniska vetenskaper
Sidor 967-76
Språk en
Länkar dx.doi.org/10.2353/ajpath.2006.0502...
Ämnesord 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
Ämneskategorier Medicin och Hälsovetenskap, Invärtesmedicin

Sammanfattning

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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