| Porphyromonas gingivalis infection during pregnancy increases maternal tumor necrosis factor alpha, suppresses maternal interleukin-10, and enhances fetal growth restriction and resorption in mice. | |
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MedLine Citation:
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PMID: 12933859 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Dongming Lin; Mary Alice Smith; Catherine Champagne; John Elter; James Beck; Steven Offenbacher |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Infection and immunity Volume: 71 ISSN: 0019-9567 ISO Abbreviation: Infect. Immun. Publication Date: 2003 Sep |
Date Detail:
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Created Date: 2003-08-22 Completed Date: 2003-09-29 Revised Date: 2013-04-18 |
Medline Journal Info:
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Nlm Unique ID: 0246127 Medline TA: Infect Immun Country: United States |
Other Details:
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Languages: eng Pagination: 5156-62 Citation Subset: IM |
Affiliation:
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Center for Oral and Systemic Diseases, School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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R0-1 DE 12453/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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