Document Detail


Immunology of preeclampsia.
MedLine Citation:
PMID:  16129952     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Preeclampsia is a placenta-dependent disorder with both local and systemic anomalies with neonatal and maternal morbidity. It is manifested late in pregnancy, but the onset is during early stages of gestation. The current hypothesis regarding the aetiology of preeclampsia is focused on maladaptation of immune responses and defective trophoblast invasion. Thus, an excessive maternal inflammatory response, perhaps directed against foreign fetal antigens, results in a chain of events including shallow trophoblast invasion, defective spiral artery remodelling, placental infarction and release of pro-inflammatory cytokines and placental fragments in the systemic circulation. During normal pregnancy, trophoblasts interact in the decidua with the unique uterine NK cells, modifying their cytokine repertoire, regulating adhesion molecules and matrix metalloproteinases. The inability of trophoblasts to accomplish these changes might be a critical factor for the onset of preeclampsia. Several cytokines, produced at the maternal-fetal interface, have an impact on trophoblast invasion. It is suggested that deficiency of interleukin-10 may contribute to enhanced inflammatory responses towards the trophoblasts elicited by e.g. tumour necrosis factor-alpha and interferon-gamma. Consequently, trophoblasts subjected to a high rate of apoptosis are hampered in their invasive capacity resulting in defective transformation of spiral arteries, hypoxia, thrombosis and infarction of the placenta. The ensuing infarction of placenta leads to leakage of increasing amounts of placental fragments and cytokines in the maternal circulation and an exaggerated systemic endothelial activation as identified in preeclampsia. So far, treatment of preeclampsia is focused on signs like hypertension, whereas attempts of modifying immune responses may be a possibility in the future.
Authors:
Leif Matthiesen; Göran Berg; Jan Ernerudh; Christina Ekerfelt; Yvonne Jonsson; Surendra Sharma
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Chemical immunology and allergy     Volume:  89     ISSN:  1660-2242     ISO Abbreviation:  Chem Immunol Allergy     Publication Date:  2005  
Date Detail:
Created Date:  2005-08-30     Completed Date:  2005-11-02     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  101183835     Medline TA:  Chem Immunol Allergy     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  49-61     Citation Subset:  IM    
Affiliation:
Department of Molecular and Clinical Medicine, Division of Obstetrics and Gynaecology, University Hospital, Linkoping, Sweden. leif.matthiesen@lio.se
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MeSH Terms
Descriptor/Qualifier:
Cytokines / metabolism
Female
Free Radicals / metabolism
Humans
Inflammation Mediators / metabolism
Killer Cells, Natural / immunology
Lymphocyte Subsets / immunology
Maternal-Fetal Exchange / immunology
Models, Immunological
Pre-Eclampsia / etiology,  immunology*
Pregnancy
Trophoblasts / immunology
Grant Support
ID/Acronym/Agency:
1 P20 RR018728/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Free Radicals; 0/Inflammation Mediators

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