PRETERM LABOR AND FETAL SEQUELAE: ROLE OF MYCOPLASMAS

早产和胎儿后遗症：支原体的作用

• 批准号: 7715872
• 负责人: MILES J. NOVY
• 金额: $ 5.55万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715872
• 关键词: Alveolus; Antibiotics; Computer Retrieval of Information on Scientific Projects Database; Count; Dinoprost; Dinoprostone; Experimental Models; Fetal Lung; Funding; Gelatinase B; Genital system; Grant; IL8 gene; Infection; Inflammatory; Institution; Interleukin-6; Interleukins; Lung diseases; Macaca mulatta; Mycoplasma; Neonatal; Patient currently pregnant; Premature Birth; Premature Labor; Prostaglandins; Research; Research Personnel; Resources; Role; Source; Tumor Necrosis Factor-alpha; Tumor Necrosis Factors; United States National Institutes of Health; Up-Regulation; Ureaplasma; Ureaplasma urealyticum biovar 1; Uterine Contraction; Work; cytokine; fetal; human TNF protein; nonhuman primate; prenatal; prevent

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We developed the first experimental model in nonhuman primates in which infection is established by intraamniotic inoculation of know quantities of lower genital tract mycoplasmas. Following experimental intraamniotic infection (IAI) with Ureaplasma parvum in long-term catheterized, pregnant rhesus monkeys, there is a sequential upregulation of proinflammatory cytokines (interleukin [IL]-1beta, tumor necrosis factor [TNF] alpha, IL-6, IL-8) prostaglandins (PGE2 and PGF2alpha), and matrix metalloproteinase-9 (MMP-9) which rise in parallel with counts for ureaplasma colonies. This is followed in all cases by uterine contraction, labor and delivery. There is associated fetal lung damage in alveoli and terminal airways. It is our working hypothesis that prenatal treatment of intrauterine U. parvum infection with appropriate antibiotics and specific inflammatory agents will inhibit preterm labor, delay premature delivery, and ameliorate or prevent fetal/neonatal lung disease.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 我们在非人类灵长类动物中开发了第一个实验模型，其中通过羊膜内接种已知数量的下生殖道支原体来建立感染。 在长期插管、怀孕的恒河猴中进行实验性羊膜内微小解脲支原体感染（IAI）后，促炎细胞因子（白细胞介素 [IL]-1β、肿瘤坏死因子 [TNF] α、IL-6、IL-6）连续上调。 8) 前列腺素（PGE2 和 PGF2α）和基质金属蛋白酶 9 (MMP-9) 与解脲支原体计数同时上升殖民地。 在所有情况下，接下来都是子宫收缩、临产和分娩。 肺泡和终末气道中存在相关的胎儿肺损伤。 我们的工作假设是，使用适当的抗生素和特定炎症剂对宫内微小 U. parvum 感染进行产前治疗将抑制早产，延迟早产，并改善或预防胎儿/新生儿肺部疾病。