Document Detail


Porphyromonas gingivalis infection during pregnancy increases maternal tumor necrosis factor alpha, suppresses maternal interleukin-10, and enhances fetal growth restriction and resorption in mice.
MedLine Citation:
PMID:  12933859     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epidemiological studies have shown a potential association between maternal periodontitis and pregnancy complications. We used a pregnant murine model to study the effect of infection with the periodontal pathogen Porphyromonas gingivalis on pregnancy outcomes. Female BALB/c mice were inoculated with heat-killed P. gingivalis (10(9) CFU) in a subcutaneous chamber and mated 2 weeks later. At gestation day (GD) 7.5, mice were challenged with live P. gingivalis (10(7) CFU) (n = 20) or broth (control; n = 8) and sacrificed at GD 16.5. Fetal growth restriction (FGR, <0.46 g) was defined as fetuses with weights 2 standard deviations (SD) smaller than controls (0.56 +/- 0.05 g [mean +/- SD]). Among the 20 challenged mice, 8 had both normal-weight (0.51 +/- 0.11 g) and FGR (0.34 +/- 0.1 g) fetuses within the same litter. All other challenged dams had normal-weight fetuses (0.57 +/- 0.04 g). Maternal liver, uterus, and spleen samples were examined for P. gingivalis DNA using a PCR technique. Of the eight challenged mice with FGR fetuses, three had PCR signals for P. gingivalis in liver and uterus, but not in the spleen. Liver, uterus, and spleen were negative for P. gingivalis DNA among all other challenged and control mice. In serum of dams with FGR fetuses, tumor necrosis factor alpha levels were elevated significantly, while interleukin-10 levels were significantly reduced compared to levels in dams with normal fetuses. P. gingivalis-specific serum immunoglobulin G levels were significantly elevated in dams with FGR fetuses compared to dams without any FGR fetuses. These data demonstrate that P. gingivalis-induced murine FGR is associated with systemic dissemination of the organism and activated maternal immune and inflammatory responses.
Authors:
Dongming Lin; Mary Alice Smith; Catherine Champagne; John Elter; James Beck; Steven Offenbacher
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Infection and immunity     Volume:  71     ISSN:  0019-9567     ISO Abbreviation:  Infect. Immun.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-22     Completed Date:  2003-09-29     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5156-62     Citation Subset:  IM    
Affiliation:
Center for Oral and Systemic Diseases, School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies, Bacterial / blood
Bacteroidaceae Infections / complications*,  immunology,  pathology
Base Sequence
DNA, Bacterial / genetics,  isolation & purification
Disease Models, Animal
Female
Fetal Growth Retardation / etiology*
Fetal Resorption / etiology*
Humans
Immunoglobulin G / blood
Interleukin-10 / metabolism*
Liver / microbiology
Maternal-Fetal Exchange
Mice
Mice, Inbred BALB C
Porphyromonas gingivalis* / genetics,  immunology,  isolation & purification
Pregnancy
Pregnancy Complications, Infectious / immunology*,  pathology
Tumor Necrosis Factor-alpha / metabolism*
Uterus / microbiology
Grant Support
ID/Acronym/Agency:
R0-1 DE 12453/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Bacterial; 0/DNA, Bacterial; 0/Immunoglobulin G; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10
Comments/Corrections

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