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Morgan R. Peltier, PhD

Associate Professor of Clinical Obstetrics, Gynecology and Reproductive Medicine


Our research evaluates the consequences of disrupting the unique immunoendocrine relationship of pregnancy where a genetically foreign tissue evades the maternal immune system by suppressing inflammation. Most of the problems in modern obstetrics including preeclampsia, preterm birth, preterm premature rupture of membranes, and placental abruption are correlated with inflammation at the maternal-fetal interface. In recent years, there has also been an increasing appreciation that exposure to infection and/or inflammation may increase the risk of autism and other neurodevelopmental disorders in the offspring. We have 2 main research areas.

1. Immunomodulatory therapies for improving pregnancy outcome. Although intra-uterine infections are frequently associated with preterm birth, the majority of the adverse outcomes appear to be associated with the host response to the infection rather than the bacteria themselves. Antibiotic therapies to prevent preterm birth have largely failed because they provide, at best, a one-time clearance of the pathogen. However, anti-inflammatory drugs such as Interleukin-10, PGJ2, antibodies to TNF-a, sulfasalazine, and carbon monoxide improved pregnancy outcomes in animal models. We are exploring how dietary factors that regulate the production of HO-1, an enzyme that produces carbon monoxide endogenously, may improve outcomes of pregnancies complicated by intrauterine infection using cell culture and animal model systems.

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2. Immunotoxicology of pregnancy. Although intrauterine infection and inflammation is a strong risk factor for preterm birth, other environmental or genetic risk factors may modify the that risk. Many environmental toxins have adverse effects on immune function and may increase the risk of preterm birth and other adverse pregnancy outcomes by enhancing the inflammatory response to ascending infections. We found that persistent organic pollutants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polybrominated diphenyl ethers (PBDEs) enhance the production of proinflammatory cytokines and/or prostaglandins by E. coli-treated placental explant cultures. Clinical studies have also suggest that women with high concentrations of organic pollutants (PBDEs or Bisphenol A) in their peripheral plasma may be at increased risk for preterm birth. We are conducting a large NIH-funded study to confirm these findings and to determine if the effects of PBDE exposure on preterm birth risk are conditional on placental infection. Given that many of these pollutants disrupt production and/or bioactivity of the thyroid hormones, we also investigating how they may increase the risk of neurodevelopmental disorders in the offspring in the presence and absence of intrauterine infection. Key papers from our lab include…


  1. Peltier MR, Koo HC, Getahun D, Menon R. Does exposure to flame retardants increase the risk for preterm birth? J Reprod Immunol 2015; 107:20-5.
  2. Peltier MR, Klimova NG, Arita Y, Gurzenda EM, Murthy A, Chawala K, Lerner V, Richardson J, Hanna N. Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta. Placenta. 2012; 33:745-9.
  3. Klimova NG, Hanna N, Peltier MR. Does carbon monoxide inhibit proinflammatory cytokine production by fetal membranes? J Perinat Med 2013; 41:683-90.
  4. Burton A, Kizhner O, Brown MB, Peltier MR. Effect of experimental genital mycoplasmosis on gene expression in the fetal brain. J Reprod Immunol. 2012; 93:9-16.