PRETERM LABOR AND FETAL SEQUELAE: ROLE OF MYCOPLASMAS

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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.