PRETERM LABOR AND FETAL SEQUELAE: ROLE OF MYCOPLASMAS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们在非人类灵长类动物中建立了第一个实验模型，在该模型中，通过羊膜内接种已知数量的下生殖道支原体来建立感染。在长期留置尿管的妊娠恒河猴实验性羊膜内微小解脲支原体感染(IAI)后，促炎症细胞因子(白介素1β、肿瘤坏死因子α、白介素6、白介素8)、前列腺素(PGE2和PGF2α)和基质金属蛋白酶-9(MMP9)的表达与解脲支原体的集落数同步升高。在所有病例中，紧随其后的是子宫收缩、分娩和分娩。在肺泡和终末呼吸道有相关的胎儿肺损伤。我们的工作假设是，产前使用适当的抗生素和特定的炎症剂治疗宫内微小解脲支原体感染可以抑制早产，推迟早产，并改善或预防胎儿/新生儿肺部疾病。

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.