help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, X.
Right arrow Articles by Jacobsson, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, X.
Right arrow Articles by Jacobsson, B.
(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.




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
X. Wang, Y. Carlsson, E. Basso, C. Zhu, C. I. Rousset, A. Rasola, B. R. Johansson, K. Blomgren, C. Mallard, P. Bernardi, et al.
Developmental Shift of Cyclophilin D Contribution to Hypoxic-Ischemic Brain Injury
J. Neurosci., February 25, 2009; 29(8): 2588 - 2596.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society for Investigative Pathology.