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. Preterm birth remains a significant economic and public health burden and the incidence is rising. Infection induced inflammation plays a significant role in preterm birth and is thought to occur as a result of infection, which promotes premature uterine contractions. Obstetrical research has yet to identify effective preventive interventions for preterm labor. The overall objective of this proposal is to develop a model system which emulates human preterm birth to ultimately elucidate molecular mechanisms of infection-induced preterm labor and related adverse neonatal sequelae (e.g. brain injury). We propose to develop a nonhuman primate model in the pigtail macaque that closely mimics an ascending lower genital tract infection at the chorio-decidual interface in the lower uterine segment-decidual interface. The central hypothesis is that infection with group B streptococcus (GBS) at the chorio-decidual interface at the proximal cervical canal will result in an inflammatory response that results in premature myometrial contractions, intra-amniotic infection, and premature delivery.
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