PRETERM LABOR AND FETAL SEQUELAE: ROLE OF MYCOPLASMAS

点击翻译按钮获取中文摘要

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.