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

Szczegóły
Abstrakt

Tytuł:: Disruption of interleukin-18, but not interleukin-1, increases vulnerability to preterm delivery and fetal mortality after intrauterine inflammation.
Autorzy:: Wang X; Perinatal Center, Department of Physiology, Göteborg University., Box 432, S-405 30 Göteborg, Sweden, and The Third Affiliated Hospital of Zhengzhou University, People's Republic of China. />Hagberg H
Mallard C
Zhu C
Hedtjärn M
Tiger CF
Eriksson K
Rosen A
Jacobsson B
Źródło:: The American journal of pathology [Am J Pathol] 2006 Sep; Vol. 169 (3), pp. 967-76.
Typ publikacji:: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: 2011-: New York : Elsevier
Original Publication: Philadelphia [etc.] American Assn. of Pathologists [etc.]
MeSH Terms:: Fetal Death/*genetics
Interleukin-1/*deficiency
Interleukin-18/*genetics
Animals ; Female ; Fetal Death/chemically induced ; Fetal Death/immunology ; Fetal Death/pathology ; Glycoproteins/immunology ; Glycoproteins/pharmacology ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Intercellular Signaling Peptides and Proteins ; Interleukin-1/immunology ; Interleukin-12/immunology ; Interleukin-18/immunology ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/toxicity ; Mice ; Mice, Knockout ; Pregnancy ; Th1 Cells/immunology ; Th1 Cells/pathology ; Uterus/immunology ; Uterus/pathology
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Substance Nomenclature:: 0 (Glycoproteins)
0 (Intercellular Signaling Peptides and Proteins)
0 (Interleukin-1)
0 (Interleukin-18)
0 (Lipopolysaccharides)
0 (interleukin-18 binding protein)
187348-17-0 (Interleukin-12)
Entry Date(s):: Date Created: 20060829 Date Completed: 20061024 Latest Revision: 20181113
Update Code:: 20240104
PubMed Central ID:: PMC1698826
DOI:: 10.2353/ajpath.2006.050207
PMID:: 16936270
: Czasopismo naukowe

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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