Document Detail


Decidual infiltration and activation of macrophages leads to early embryo loss.
MedLine Citation:
PMID:  9228304     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PROBLEM: There is considerable controversy concerning the root cause and mechanisms of early embryo loss. It has been suggested that most pregnancy losses occur due to morphogenetic anomalies of the embryo. It has also been suggested that the maternal specific immune system rejects the embryo. METHODS: Existing data on the cell and molecular biology of early embryo loss in murine experimental models is reviewed. RESULTS: Using the CBA(female) x DBA/2(male) model of early embryo loss, it has been established that maternal inflammatory cells infiltrate the decidua basalis of all implantation sites within 48 hr after implantation. For most embryos, the relatively low numbers of macrophages (Mphi) and natural killer-like (NK-like) cells of maternal origin remain relatively constant after day 8, whereas 20-30% of the embryos show a significant increase in inflammatory cells in the maternal decidua, corresponding to the incidence of early embryo resorption visible at day 12. Evidence will be reviewed to suggest that decidual NK-like cells are not cytolytic but may be producing the Mphi-activating cytokine interferon gamma (IFN-gamma), which activates decidual Mphi and other cells. Furthermore, embryo loss is ameliorated by in vivo treatment with anti-IFNgamma or anti-NK antisera, indicating that NK-like cells and/or IFNgamma are required for embryo loss, but not for embryo survival. In resorbing embryos, the inflammatory Mphi show evidence of having been primed during early pregnancy, in that in vitro incubation with lipopolysaccharide induced the production of tumor necrosis factor alpha and nitric oxide. CONCLUSION: These findings support the concept that early embryo loss is a nonspecific event mediated by the triggering of cytotoxin production by primed decidual macrophages.
Authors:
M G Baines; A J Duclos; E Antecka; E K Haddad
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of reproductive immunology (New York, N.Y. : 1989)     Volume:  37     ISSN:  1046-7408     ISO Abbreviation:  Am. J. Reprod. Immunol.     Publication Date:  1997 Jun 
Date Detail:
Created Date:  1997-10-09     Completed Date:  1997-10-09     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8912860     Medline TA:  Am J Reprod Immunol     Country:  DENMARK    
Other Details:
Languages:  eng     Pagination:  471-7     Citation Subset:  IM    
Affiliation:
Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Crosses, Genetic
Cytotoxicity, Immunologic
Decidua / pathology*
Female
Fetal Resorption / etiology*,  pathology
Gene Expression Regulation, Developmental
Gestational Age
Interferon-gamma / biosynthesis,  genetics
Killer Cells, Natural / immunology,  secretion
Lymphocyte Activation
Macrophage Activation*
Macrophages / immunology
Male
Mice
Mice, Inbred C3H
Mice, Inbred CBA
Mice, Inbred DBA
Nitric Oxide / biosynthesis
Nitric Oxide Synthase / biosynthesis,  genetics
Pregnancy
Tumor Necrosis Factor-alpha / biosynthesis,  genetics
Chemical
Reg. No./Substance:
0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide; 82115-62-6/Interferon-gamma; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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