Document Detail


Porphyromonas gingivalis infection in pregnant mice is associated with placental dissemination, an increase in the placental Th1/Th2 cytokine ratio, and fetal growth restriction.
MedLine Citation:
PMID:  12933860     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our previous animal studies showed that maternal Porphyromonas gingivalis infection in a subcutaneous chamber is associated with hepatic and uterine translocation, as well as systemic induction of maternal inflammatory responses, both of which were associated with fetal growth restriction (FGR). However, P. gingivalis-challenged dams had fetuses with either FGR (2 standard deviations below mean weight of nonchallenged dams) or normal weight. Therefore, the objective of this study was to determine whether maternal infection with P. gingivalis compromises normal fetal development via direct placental invasion and induction of fetus-specific placental immune responses characterized by a proinflammatory Th1-type cytokine profile. P. gingivalis-specific DNA was detected in placentas and fetuses of FGR and normal littermates from P. gingivalis-infected dams. Th1- and Th2-type cytokine mRNA as well as tumor necrosis factor alpha and transforming growth factor beta 2 mRNA were examined in placental tissue by using reverse transcription-PCR to determine Th1/Th2 ratios. For eight litters containing both normal-weight and FGR fetuses, P. gingivalis DNA was detected only in the placentas of FGR fetuses. All fetuses and all amniotic fluid samples from infected and control dams were negative for P. gingivalis DNA. mRNA levels of gamma interferon and interleukin-2 (IL-2) were significantly increased in placentas of FGR fetuses, while expression of IL-10 was significantly decreased in the same group. These data indicate that, in P. gingivalis-challenged dams, within each litter there is placenta-specific translocation of P. gingivalis that results in growth restriction of the targeted fetus, which is associated with a shift in the placental Th1/Th2 cytokine balance.
Authors:
Dongming Lin; Mary Alice Smith; John Elter; Catherine Champagne; Christine Lynn Downey; James Beck; Steven Offenbacher
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:  5163-8     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
Bacteroidaceae Infections / complications*,  immunology,  microbiology,  pathology
Cytokines / genetics
Female
Fetal Growth Retardation / etiology*
Gene Expression
Maternal-Fetal Exchange
Mice
Placenta / immunology,  microbiology
Porphyromonas gingivalis* / genetics,  immunology,  isolation & purification
Pregnancy
Pregnancy Complications, Infectious / immunology*,  microbiology*,  pathology
RNA, Messenger / genetics,  metabolism
Th1 Cells / immunology
Th2 Cells / immunology
Grant Support
ID/Acronym/Agency:
R0-1 DE 12453/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/RNA, Messenger
Comments/Corrections

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