ORAL CONDITIONS AND PREGNANCY--NEONATAL OUTCOMES

口腔状况与妊娠——新生儿结局

• 批准号: 6654099
• 负责人: RICHARD L AUTEN
• 金额: $ 10.81万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6654099
• 关键词: biomarker; bronchopulmonary dysplasia; clinical research; colitis; cytokine; disease /disorder proneness /risk; female; genetic polymorphism; heart disorder; hemorrhage; human pregnant subject; human subject; inflammation; medical complication; oral health; periodontitis; periodontium disorder; pregnancy immunology; pregnancy infection; premature infant human; prenatal stress

This supplemental application extends the evaluation of oral inflammation and infection, effects on pregnancy to the potential impact on premature newborns and the leading complications of prematurity, lung and brain damage. The general hypothesis is that subclinical infection, possibly originating in periodontal disease, affects the inflammatory and immune responses in women, placing them at higher risk for preterm labor and delivery. Pro-inflammatory cytokines, associated with periodontal disease and intrauterine infection, have been implicated in the initiation of preterm labor. Our proposed studies will assess how these maternal processes affect the inflammatory cascade in the premature low birth eight infant and the risk for inflammatory complication of prematurity. Prenatal infection and inflammation are associated with brain injury in premature newborns, in particular intraventricular hemorrhage and periventricular leukomalacia. Inflammatory cytokines are found in the tracheal secretions of premature newborns who later develop bronchopulmonary dysplasia. Necrotizing enterocolitis is another serious life-threatening complication of prematurity associated with elevations in pro-inflammatory cytokines. Genetic polymorphisms encoding IL-1beta and TNFalpha are associated with increased cytokine expression and may predispose to an exaggerated inflammatory response. We will measure pro-inflammatory cytokines in pregnant women and compare them to those in their premature newborns. Cytokines will be correlated with the inflammatory complications of prematurity: bronchopulmonary dysplasia, intraventricular hemorrhage/periventricular leukomalacia, and necrotizing enterocolitis, using logistic regression analysis. Polymorphisms will be identified and correlated with these inflammatory complications with the abundance of cytokine protein and mRNA in tracheal aspirates cells and in blood. We will test whether a panel of mediators identified at risk with high sensitivity and specificity. Our long-term aim is to develop markers that identify newborns at highest risk and provide the basis for future therapy to prevent these complications of prematurity.

该补充申请将口腔炎症和感染的评价、对妊娠的影响扩展到对早产儿的潜在影响以及早产、肺和脑损伤的主要并发症。一般的假设是，亚临床感染，可能起源于牙周病，影响妇女的炎症和免疫反应，使他们在早产和分娩的风险更高。与牙周病和宫内感染相关的促炎细胞因子与早产的发生有关。我们提出的研究将评估这些母体过程如何影响早产低产8个婴儿的炎症级联反应和早产炎症并发症的风险。产前感染和炎症与早产儿脑损伤有关，特别是脑室内出血和脑室周围白质软化。炎症性细胞因子存在于早产儿的气管分泌物中，这些早产儿后来发展为支气管肺发育不良。坏死性小肠结肠炎是早产儿的另一种严重危及生命的并发症，与促炎细胞因子升高有关。编码IL-1 β和TNF α的遗传多态性与细胞因子表达增加相关，并可能使炎症反应加剧。我们将测量孕妇的促炎细胞因子，并将其与早产儿的促炎细胞因子进行比较。使用逻辑回归分析，细胞因子将与早产的炎性并发症相关：支气管肺发育不良、脑室内出血/脑室周围白质软化和坏死性小肠结肠炎。将鉴定多态性并将其与这些炎症并发症与气管吸出物细胞和血液中细胞因子蛋白和mRNA的丰度相关联。我们将测试一组介质是否具有高敏感性和特异性。我们的长期目标是开发识别高危新生儿的标志物，并为未来预防早产儿并发症的治疗提供基础。