Increased TLR4 expression in murine placentas after oral infection with periodontal pathogens.
Increased TLR4 expression in murine placentas after oral infection with periodontal pathogens.
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DOI：
10.1016/j.placenta.2008.11.017
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发表时间：
2009-02
期刊：
影响因子：
3.8
通讯作者：
Offenbacher S
中科院分区：
文献类型：
--
作者：
Arce RM;Barros SP;Wacker B;Peters B;Moss K;Offenbacher S
母体牙周炎已成为人类早产的一个假定危险因素。牙周炎相关的牙齿生物膜被认为是口腔细菌和相关毒力因子的重要来源，这些毒力因子通过血液传播并影响胎儿胎盘单位;然而，其潜在的生物学机制尚未完全阐明。本研究假设，口腔感染的人牙周病原体弯曲杆菌直和牙龈卟啉单胞菌能够诱导胎儿生长受限，胎盘炎症和增强Toll样受体4型（TLR 4）的表达在小鼠妊娠模型。雌性Balb/C小鼠（n=40）经口感染C.直肌和/或牙龈卟啉单胞菌，并每周交配一次。在胚胎第16.5天处死妊娠小鼠，收集胎盘并通过真实的时间PCR和免疫荧光分析TLR 4 mRNA水平和定性蛋白表达。TLR 4 mRNA表达在C.直肌感染组与对照组相比（1.98±0.886倍差异，P<0.01，ANOVA）。小鼠胎盘显微镜分析显示滋养层中TLR 4的免疫荧光增强，主要在胎盘迷路层中。此外，合并口腔感染与C。与对照组相比，直肌和牙龈卟啉单胞菌显著降低了总体繁殖力（感染与未感染小鼠分别为16.7%与75%，P=0.03，Kaplan-Meier）。结果支持牙周病原体感染后胎盘TLR 4表达增强。TLR 4通路与早产的发病机制有关，因此胎盘TLR 4的异常调节可能为了解母体牙周炎和牙周病原体与胎盘炎症和早产发病机制的关系提供新的见解。
Maternal periodontitis has emerged as a putative risk factor for preterm births in humans. The periodontitis-associated dental biofilm is thought to serve as an important source of oral bacteria and related virulence factors that hematogenously disseminate and affect the fetoplacental unit; however the underlying biological mechanisms are yet to be fully elucidated. This study hypothesized that an oral infection with the human periodontal pathogens Campylobacter rectus and Porphyromonas gingivalis is able to induce fetal growth restriction, placental inflammation and enhance Toll-like receptors type 4 (TLR4) expression in a murine pregnancy model. Female Balb/C mice (n=40) were orally infected with C. rectus and/or P. gingivalis over a 16-week period and mated once per week. Pregnant mice were sacrificed at embryonic day (E) 16.5 and placentas were collected and analyzed for TLR4 mRNA levels and qualitative protein expression by real time PCR and immunofluorescence. TLR4 mRNA expression was found to be increased in C. rectus-infected group (1.98±0.886 fold difference, P<0.01, ANOVA) compared to controls. Microscopic analysis of murine placentas showed enhanced immunofluorescence of TLR4 in trophoblasts, mainly in the placental labyrinth layer. Also, combined oral infection with C. rectus and P. gingivalis significantly reduced the overall fecundity compared to controls (16.7% vs. 75%, infected vs. non-infected mice respectively, P=0.03, Kaplan-Meier). The results supported an enhanced placental TLR4 expression after oral infection with periodontal pathogens. The TLR4 pathway has been implicated in the pathogenesis of preterm births; therefore the abnormal regulation of placental TLR4 may give new insights into how maternal periodontitis and periodontal pathogens might be linked to placental inflammation and preterm birth pathogenesis.
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影响因子：
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作者：
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通讯作者：
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