The microbiome modulates inflammation at the fetal maternal interface on both term and preterm labor. Inflammophilic oral bacteria, such as Porphyromonas gingivalis, as well as urogenital microorganisms (UGM) could translocate to the placenta and activate immune mechanisms in decidual tissue that is associated with adverse pregnancy outcomes (APO). This study establishes the associations between the presence of microbes in the placenta and placental cytokine patterns in women who presented APO, e.g., low birth weight (LBW), preterm premature rupture of membranes (PPROM), preterm birth (PTB) and other clinical signs related to Chorioamnionitis (CA). A total of 40 pregnant women were included in the study and divided into five groups according to placental infection (PI) and APO, as follows: (1) women without PI and without APO (n = 17), (2) women with P. gingivalis-related PI and APO (n = 5), (3) women with P. gingivalis-related PI and without APO (n = 4), (4) women with PI related to UGM and APO (n = 5) and (5) women without PI with APO (n = 9). Obstetric, clinical periodontal status evaluation, and subgingival plaque sampling were performed at the time of delivery. Placental levels of interleukin IL-1β, IL-6, IL-10, IL-15, IL-17A, IL-17F, IL-21, IL-12p70, tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 α (MCP-1α), granzyme B, and interferon-γ (IFN-γ) were determined using a multiplex flow cytometry assay. All patients showed a predominant Th-1 cytokine profile related to labor, characterized by IFN-γ overexpression. The analysis by groups suggests that Th-1 profile was trending to maintain cytotoxic cell activity by the expression of IL-15 and granzyme B, except for the group with P. gingivalis-related PI and APO, which exhibited a reduction of IL-10 and IL-17F cytokines (p < 0.05) and a Th-1 profile favoring macrophage activation by MCP-1 production (p < 0.05). This study confirms a pro-inflammatory pattern associated with labor, characterized by a Th-1 profile and the activity of cytotoxic cells, which is enhanced by PI with UGM. However, PI associated with P. gingivalis suggests a switch where the Th-1 profile favors an inflammatory response mediated by MCP-1 and macrophage activity as a mechanistic explanation of its possible relationship with adverse outcomes in pregnancy.

微生物组可在足月和早产时调节胎儿母体界面处的炎症。嗜血性口腔细菌，例如牙龈卟啉单胞菌以及泌尿生殖道微生物（UGM）可能易位至胎盘并激活与不良妊娠结局（APO）相关的蜕膜组织中的免疫机制。这项研究建立了存在APO的女性的胎盘中微生物的存在与胎盘细胞因子类型之间的关联，例如低出生体重（LBW），胎膜早破（PPROM），早产（PTB）和其他临床体征与绒毛膜羊膜炎（CA）有关。研究共纳入40名孕妇，并根据胎盘感染（PI）和APO分为五组：（1）没有PI和APO的妇女（ñ = 17），（2）女性 牙龈卟啉单胞菌相关的PI和APO（ñ = 5），（3）名女性 牙龈卟啉单胞菌相关的PI，并且没有APO（ñ = 4），（4）与UGM和APO相关的PI的女性（ñ = 5）和（5）没有APO的PI的女性（ñ= 9）。分娩时进行产科，临床牙周状况评估和龈下斑块采样。胎盘白细胞介素IL-1β，IL-6，IL-10，IL-15，IL-17A，IL-17F，IL-21，IL-12p70，肿瘤坏死因子-α（TNF-α），单核细胞趋化蛋白使用多重流式细胞术测定了-1α（MCP-1α），颗粒酶B和干扰素-γ（IFN-γ）。所有患者均显示出与分娩有关的主要Th-1细胞因子谱，其特征为IFN-γ过表达。按组进行的分析表明，除了具有下列特征的组外，Th-1分布倾向于通过IL-15和颗粒酶B的表达来维持细胞毒性细胞的活性。牙龈卟啉单胞菌相关的PI和APO，它们可降低IL-10和IL-17F细胞因子（p <0.05）和Th-1分布，有利于通过MCP-1产生激活巨噬细胞（p<0.05）。这项研究证实了与分娩有关的促炎模式，其特征在于Th-1分布和细胞毒性细胞的活性，而UGM的PI可以增强这种活性。但是，PI与牙龈卟啉单胞菌 提示Th-1分布倾向于由MCP-1和巨噬细胞活性介导的炎症反应，这是其与妊娠不良结局可能关系的机械解释。