title: Porphyromonas gingivalis infection in pregnant mice is associated with placental dissemination, an increase in the placental Th1/Th2 cytokine ratio, and fetal growth restriction.
abstract: 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.affiliation: Center for Oral and Systemic Diseases, School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
authors.forename: Dongming
authors.initials: D
authors.lastname: Lin
authors.forename: Mary Alice
authors.initials: MA
authors.lastname: Smith
authors.forename: John
authors.initials: J
authors.lastname: Elter
authors.forename: Catherine
authors.initials: C
authors.lastname: Champagne
authors.forename: Christine Lynn
authors.initials: CL
authors.lastname: Downey
authors.forename: James
authors.initials: J
authors.lastname: Beck
authors.forename: Steven
authors.initials: S
authors.lastname: Offenbacher
mesh_terms: D000818:Animals; D016866:Bacteroidaceae Infections / Q000150:complications* / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000235:genetics; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology*; D015870:Gene Expression; D008431:Maternal-Fetal Exchange; D051379:Mice; D010920:Placenta / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016207:Cytokines; D012333:RNA, Messenger