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: 7348876
• 负责人: MILES J. NOVY
• 金额: $ 7.68万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7348876
• 关键词: PRETERM; LABOR; FETAL; SEQUELAE; ROLE

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 the intraamniotic inoculation of known quantities of the genital organisms Ureaplasma urealyticum or Mycoplasma hominis. Following experimental intraamniotic infection (IAI) in chronically-catheterized, pregnant rhesus monkeys, there is a sequential upregulation of proinflammatory cytokines (interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha, IL-6, IL-8), prostaglandin (PG)E2 and PGF2alpha, and matrix metalloproteinase-9 (MMP-9). This is followed in all cases by uterine contraction, labor and delivery. Intraamniotic cytokine and (PG) concentrations rise in parallel with counts for genital mycoplasma colonies. Associated fetal lung damage in alveoli and terminal airways is more severe with U. urealyticum than with M. hominis infection. It is our working hypothesis that prenatal treatment of intrauterine U. urealyticum or M. hominis infection with appropriate antibiotics and specific anti-inflammatory agents will inhibit preterm labor, delay premature delivery, and ameliorate or prevent fetal/neonatal lung disease.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。我们在非人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生殖器有机体解脲脲原体或人型支原体来建立感染。在长期插管的妊娠恒河猴中，实验性羊膜内感染（IAI）后，促炎细胞因子（白细胞介素（IL）-1 β、肿瘤坏死因子（TNF）α、IL-6、IL-8）、前列腺素（PG）E2和PGF 2 α以及基质金属蛋白酶-9（MMP-9）依次上调。在所有情况下，子宫收缩，分娩和分娩都是如此。羊膜腔内细胞因子和（PG）浓度与生殖道支原体菌落计数平行升高。相关的胎儿肺损伤的肺泡和终端气道是更严重的U。溶脲支原体的感染率高于溶脲支原体。人类感染我们的工作假设是，产前治疗宫内U。解脲支原体或M.使用适当的抗生素和特异性抗炎剂的人感染将抑制早产、延迟早产、并改善或预防胎儿/新生儿肺病。