PRETERM LABOR AND FETAL SEQUELAE: ROLE OF MYCOPLASMAS

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 我们在非人灵长类动物中建立了第一个实验模型，通过羊膜内接种已知数量的下生殖道支原体建立感染。 在长期插管的妊娠恒河猴中，实验性羊膜内感染（IAI）微小脲原体后，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（PGE 2和PGF 2 α）和基质金属蛋白酶-9（MMP-9）依次上调，并与脲原体菌落计数平行升高。 在所有情况下，子宫收缩，分娩和分娩都是如此。 在肺泡和终末气道中存在相关的胎肺损伤。 我们的工作假设是，产前治疗宫内U。用适当的抗生素和特异性炎症剂治疗细小病毒感染将抑制早产、延迟早产、并改善或预防胎儿/新生儿肺病。

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.