Peta L. Grigsby

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Today more than 1,400 babies in the United States (1 in 8) will be born prematurely. But what does the future hold for these babies? Many survivors grow up healthy; others aren't so lucky. Even the best care cannot always spare a premature baby from lasting disabilities such as cerebral palsy, mental retardation or learning problems, chronic lung disease, and vision/hearing impairments. In fact, half of all neurological disabilities in children are related to preterm birth.

Preterm labor resulting in premature birth (<37 weeks' gestation) is arguably the most important unresolved public health issue in obstetric medicine in the developed world today and remains the leading cause of neonatal morbidity and mortality. Despite our ability to care for these neonates, the prematurity rates continue to rise (16% increase over the past decade). Preterm labor is a syndrome initiated by multiple causes, however a growing body of evidence indicates that maternal lower genital tract infections are a major cause of preterm birth, especially the birth of the most immature infants (<28 weeks gestation). Among bacterial pathogens, genital mycoplasma species (i.e., Ureaplasma urealyticum and Ureaplasma parvum) are the most prevalent and play a unique role in causing and/or contributing to adverse obstetrical outcomes at nearly every stage of pregnancy. Isolation of Ureaplasma species from the placental membranes and amniotic fluid has consistently been associated with chorioamnionitis, preterm birth, and adverse perinatal outcomes, such as chronic lung disease and neurodevelopmental impairment. Infants born prematurely have higher rates of childhood learning disabilities, cerebral palsy, sensory deficits and respiratory illnesses. These negative health and developmental effects of preterm birth often extend to later life resulting in enormous medical, educational, psychological and social costs (estimated to exceed $26 billion annually).

Peta L. Grigsby, PhD  heads the Pregnancy and Perinatal Research Group in the Division of Reproductive Sciences at the ONPRC. The perinatal research group has established a unqiue nonhuman primate model in which to study the inflammatory pathways (maternal and fetal endocrine-immune interactions) that cause preterm labor and novel diagnostic biomarkers and therapuetic interventions for preterm labor associated with reproductive tract Ureaplamsa infections and for the prevention of fetal and neonatal injury (i.e., cerebral white matter damage and lung injury). Our experimental data in the rhesus monkey demonstrate that U.parvum as a sole pathogen in the amniotic cavity elicits a robust fetal inflammatory response and causes neuropathologic abnormalities consistent with early stages of periventricular white matter damage, in addition to fetal lung injury. The eradication of intra-amniotic ureaplasma from fetal tissues by maternal antibiotic therapy in our experimental model, demonstrates the biological plausability of reducing lung injury and brain inflammation in utero and by extension reduce the risk of neonatal bronchopulmonary dysplasia and adverse neurological consequences (i.e., neurodevelopmental disabilities, including cerebral palsy).

Dr. Grigsby and colleagues recently expanded the infant care facilities at the ONPRC with the addition of a specialized intensive care nursery, marking the beginning of a new era in their preterm birth studies and enabling their investigations to bridge the gap between maternal-fetal obstetrics and pediatric medicine. This one-of-a kind specialized nursery is designed to support postnatal survival of preterm rhesus monkeys exposed to Ureaplasma intra-amniotic infection and antimicrobial therapy in utero. In collaboration with the Behavioral Services Unit at ONPRC, Dr. Grigsby's research team are performing serial assessments of neurobehavioral and cognitive development (i.e., reflexive behavior, sensorimotor function and visual alertness) of preterm infants to obtain critical data on the effectiveness and safety of treating intra-amniotic infections while the fetus remains in utero. They anticipate that their studies (which represent the first direct and comprehensive assessment of maternal antibiotic therapeutic interventions for preterm labor in the setting of intra-amniotic infection) will delay preterm birth, ameliorate fetal and neonatal lung disease, and decrease the risk of neurologic impairment.

Dr. Grigsby's research program has evolved through expanded multidisciplinary collaboration among clinician scientists with neonatology and pediatric specialties and basic scientists with expertise in microbiology, reproductive immunology, pathology and cardiovascular physiology. In this regard, her field of research has expanded from preterm birth studies to now include studies on placental development and fetal growth. This research initiative seeks to understand the ability of the developing placental to respond to an adverse in utero environment and to determine the mechanisms underlying placental plasticity which are at the root of the Developmental Origins of Adult Disease phenomenon. This work is providing the essential ground work for our future understanding of the mechanisms of programmed disease. A better understanding of placental plasticity will provide a basis for developing interventional strategies to improve placental function either through increased nutrient transport supply and/or vascular supply (i.e., increase umbilical blood flow) when placental insufficiency is clinically evident.  



Dr. Peta Grigsby received her B.Sc (Hons) in Physiology, Pharmacology and Biochemistry from Monash University, Melbourne, Australia in 1998. She obtained her doctorate degree in Fetal and Neonatal Physiology at Monash University in 2002. During her graduate tenure Dr. Grigsby studied various mechanisms which lead to preterm labor, specifically she focused on the role of prostaglandins in the initiation of normal and preterm labor. Dr. Grigsby's post-doctoral fellowship (2003-2006), was completed in the Department of Obstetrics and Gynecology, Division of Maternal and Fetal Medicine, University of Cincinnati, OH. Here she focused on characterizing the temporal and tissue specific localization and expression of PGE2 receptor subtypes and the PGF2 receptor, in human myometrium, amnion and choriodecidua during pregnancy, at a variety of gestational ages. The regulation of these receptors by progesterone, estrogen and cytokines was also investigated using a cultured human myometrial cell line (ULTR) and a hormonally manipulated pregnant rat model. Dr. Grigsby is currently appointed as an Assistant Scientist at the ONPRC, Division of Reproductive & Developomental Sciences and holds a joint appointment as an Assistant Research Professor in the Department of Obstetrics and Gynecology at the Oregon Health & Science University.



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Acosta EP, Grigsby PL, Larson KB, James AM, Long MC, Duffy LB, Waites KB, Novy MJ. (2013) Transplacental Transfer of Azithromycin and Its Use for Eradicating Intra-amniotic Ureaplasma Infection in a Primate Model. J. Infect Dis. Epub. PMID: 24179112

Grigsby PL, Novy MJ, Sadowsky DW, Morgan T, Long MC, Acosta E and Waites KB. (2012). Maternal Azithromycin Therapy for Ureaplasma Intra-amniotic Infection Delays Preterm Delivery and Reduces Fetal Lung Injury in a Primate Model. Am J Obstet Gyn. Editor’s Choice Article. Epub. PMC3505245

Schelonka RL, Grigsby PL, Roberts V and McEvoy C. (2012). The Ureaplasma Conundrum: should we look or ignore? In: Hematology, Immunology and Infectious Disease: Neonatology Questions and Controversies; Role of ureaplasmal infection in inflammation and collateral end organ injury. Eds, Robin K Ohls, MD and Akhil Maheshwari, Saunders and Elsvier 2nd edition: ISBN:978-4377-2662-6; Chapter 15:253-267.

Roberts VH, Räsänen JP, Novy MJ, Frias A, Louey S, Morgan TK, Thornburg KL,Spindel ER, Grigsby PL. (2012). Restriction of placental vasculature in a non-humanprimate: a unique model to study placental plasticity. Placenta. 33:73-6. Epub. PMC3248988


See a full listing of Dr. Grigsby's publications