Abstract
Trophoblast participates in preventing allorecognition and controlling pathogens that compromise fetal wellbeing. Toll-like receptors recognize conserved sequences on the pathogens surface and trigger effector cell functions. Porphyromonas gingivalis is thought to spread to the umbilical cord and cause fetal growth restriction. Objective: To characterize expression and function of TLR-2 and TLR-4 in trophoblast cells from Porphyromonas gingivalisinfected pregnant rats. Methods: Live Porphyromonas gingivalis were challenged into the maxillary first molar subgingival sulcus of female rats before and/or during pregnancy and sacrified on gestational day (GD) 14 and 20. Porphyromonas gingivalis was detected by API-ZYM system in the maternal blood of the retro-orbital venous plexus and the umbilical cord. TLR-2 and TLR-4 expressions in trophoblast cells was detected by immunohistochemistry. Results: Porphyromonas gingivalis was first detected in the maternal blood and finally spread to the umbilical cord. Syncytiotrophoblast, spongitrophoblast and trophoblastic giant cell in treated groups had significantly higher expression of TLR-2 and TLR-4 than control group (p<0.05). Conclusion: Syncytiotrophoblast, spongitrophoblast and trophoblastic giant cell are able to recognize Porphyromonas gingivalis through TLR-2 and TLR-4 expression. The ligation of TLR-2 and TLR-4 promoted cytokine production and induced trophoblast cell death. These findings strengthen links between periodontal disease and fetal growth restriction. DOI: 10.14693/jdi.v20i2.150
Highlights
The growth and survival of fetus is dependent on placenta, which forms the interface of feto-maternal circulation, facilitates metabolism, gas exchange, and waste disposal of the fetus
The subjects of study were consisted of two blocks, they were sacrificed on gestational day (GD) 14 and GD 20
Each block was subdivided into four groups, which consisted of (1) the control group, no Porphyromonas gingivalis infection; (2) the Pg-BD group, an infection of Porphyromonas gingivalis before and during pregnancy; (3) the Pg-B group, an infection of Porphyromonas gingivalis before pregnancy; and (4) the Pg-D group, an infection of Porphyromonas gingivalis during pregnancy
Summary
The growth and survival of fetus is dependent on placenta, which forms the interface of feto-maternal circulation, facilitates metabolism, gas exchange, and waste disposal of the fetus. The placenta produces hormones that altered maternal physiology during pregnancy and forms a barrier against the maternal immune system.[1] Murine placenta consists of three layers, decidual zone, juntional zone and labyrinth zone. Labyrinth zone consists of branched villi designed for the efficient exchange of nutrients.[2] Maternal and fetal blood flows are adversely in the labyrinth to maximize the transport of nutrients.[3] If thelabyrinthdoes not obtain the proper pattern, branching and dilatation of vascularization, perfused placenta will be disrupted, resulted in poor oxygen and nutrients diffusion.[4]
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