I am a scientist with almost eighteen years of experience in basic and translational research. I received my Ph.D. in animal molecular biology and cellular biology at the University of Florida in 2000 where I worked in Dr. Peter J. Hansen’s laboratory on reproductive immunology (http://www.animal.ufl.edu/hansen). My dissertation work focused on the protein chemistry, immunoregulatory activity, and molecular phylogeny of uterine serpins-a group of proteins produced by the endometrium in response to progesterone that suppress immunity in the gravid uterus to help permit the survival of the fetal allograft. Upon graduation I joined Dr. Mary B. Brown’s laboratory and began to work with genital mycoplasmas, the most frequent pathogens of the human reproductive tract and are through to cause many adverse pregnancy outcomes such as preterm birth by stimulating inflammation. I continued working on intrauterine infections and the host-response at my first academic appointment in the Department of Obstetrics and Gynecology at the University of Utah where I worked closely with Dr. Barry C. Cole, on the virulence factors of Mycoplasma spp., to characterize novel proinflammatory components of M. hominis, U. urealyticum, M. arthritidis and M. pulmonis. In 2004, I joined the Department of Obstetrics and Gynecology at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School. There I ran the Perinatal Biology Laboratory and frequently collaborated with Dr. Cande V. Ananth on epidemiology projects. In late 2008, I came to Winthrop University Hospital, where I direct the laboratory for Women’s and Children’s Research Institute.
Description of Research Interests/Activities
Our laboratory takes a multidisciplinary approach to investigating methods to diagnose, treat and preventing preterm birth. Preterm birth is defined as delivery of the baby before 37 completed weeks of gestation (beginning with the last menstrual period). It is the foremost problem in modern obstetrics and affects about 1 in every 8 pregnancies. Even with all advances in neonatology that have occurred over the years, preterm birth is still the leading cause of infant morbidity and mortality.
Over the past decade there has been an increased understanding of the role that immunity plays in the pathology of most preterm births. Pregnancy has always intrigued immunologists for generations because it is the one exception to the rule that transplanted tissues must be genetically matched between donors and recipients. The placenta plays an active role in controlling maternal immunity in the uterus to ensure that it does not become recognized as foreign tissue and targeted for destruction. However, environmental triggers such as bacterial infections, maternal stress or toxicants can induce inflammation in uterus and placenta. This overrides the placental control of maternal immunity and activates the labor mechanism which may function to empty the uterus of the infection in an attempt to save the mother at the cost of her baby.
Our laboratory has had a special emphasis on the bacteria that are responsible for the majority of these intrauterine infections, the genital mycoplasmas. Mycoplasmas are a distinct type of bacteria that is highly adapted for living on mucosal surfaces such as the genital tract and the lungs. They lack cell walls and have some of the smallest genomes known for free-living organisms (they are literately the lowest form of life). They are resistant to common antibiotics such as penicillin and other types of antibiotics merely slow down their growth so they can be difficult infections to clear from the mother. Our lab has taken isolated some of the components of these organisms that stimulate the inflammatory immune response that is so detrimental to pregnancy and characterized their interactions with the maternal immune system.
Another major effort by our lab is to study novel anti-inflammatory strategies for preventing preterm birth. Inflammation is a common component of disease processes including arthritis, neurdegerative diseases, diabetes and cardiology and a number of drugs have been designed to treat these diseases by suppressing inflammation. We are currently working to study whether some of these same compounds can be used to prevent preterm birth. Some of these anti-inflammatory compounds are available as nutritional supplements and may be safe enough for use in women who are traditionally considered to be a low risk for preterm birth (those who have never been pregnant or who have only had a previous term birth). Such women are not targeted for aggressive interventions by obstetrician because the rate of preterm birth in this population is very low (about 4%). However, due to the fact that these women comprise the bulk of clinical practice, they account for over 90% of preterm births nation-wide. Therefore, we a exploring dietary strategies that are safe enough to be applied to all women that will It is our goal to develop improved nutritional guidelines for these women that will minimize their risk of having a preterm birth.
Areas of Experience
Research Team Members
Ellen Gurzenda, B.S. Laboratory Technician Hschi-Chi Koo, M.S. Senior Research Associate Yuko Arita, D.D.S., Ph.D. Senior Research
Associate Natalia Klimov, Research Assistant
Clinical Practice and Interests
Pregnancy Biology and its complications
Nath CA, Ananth CV, Smulian JC, Peltier MR. Can sulfasalazine prevent
infection-mediated pre-term birth in a murine model? Am J Reprod Immunol. 2010
Feb;63(2):144-9. Epub 2009 Dec 20. PubMed PMID: 20039863.
Peltier MR, Faux DS, Hamblin SD, Silver RM, Esplin MS. Cytokine production by
peripheral blood mononuclear cells of women with a history of preterm birth. J
Reprod Immunol. 2010 Jan;84(1):111-6. Epub 2009 Dec 14. PubMed PMID: 20005575.
Menon R, Peltier MR, Eckardt J, Fortunato SJ. Diversity in cytokine response
to bacteria associated with preterm birth by fetal membranes. Am J Obstet
Gynecol. 2009 Sep;201(3):306.e1-6. PubMed PMID: 19733282.
Peltier MR, Ananth CV, Oyelese Y, Vintzileos AM; New Jersey-Placental
Abruption Study Investigators. Thromboembolic diseases in families of women with
placental abruption. Epidemiology. 2009 Sep;20(5):733-7. PubMed PMID: 19535986.
Peltier MR, Faux DS, Hamblin SD, Cooper C, Silver RM, Esplin MS. Effect of
aspirin treatment on TNFalpha production by women with a history of preterm
birth. J Reprod Immunol. 2009 Jun;80(1-2):109-14. Epub 2009 May 5. PubMed PMID:
Peltier MR, Berlin Y, Tee SC, Smulian JC. Does progesterone inhibit
bacteria-stimulated interleukin-8 production by lower genital tract epithelial
cells? J Perinat Med. 2009;37(4):328-33. PubMed PMID: 19290856.
Peltier MR, Tee SC, Kinzler WL, Smulian JC. Effect of sulfasalazine on basal
and bacteria-stimulated interleukin-8 production by endocervical epithelial
cells. Am J Reprod Immunol. 2009 Mar;61(3):190-5. PubMed PMID: 19239421.
Peltier MR, Tee SC, Smulian JC. Effect of progesterone on proinflammatory
cytokine production by monocytes stimulated with pathogens associated with
preterm birth. Am J Reprod Immunol. 2008 Oct;60(4):346-53. PubMed PMID: 19046141.
Ananth CV, Peltier MR, Moore DF, Kinzler WL, Leclerc D, Rozen RR; New
Jersey-Placental Abruption Study Investigators. Reduced folate carrier 80A–>G
polymorphism, plasma folate, and risk of placental abruption. Hum Genet. 2008
Sep;124(2):137-45. Epub 2008 Jul 16. PubMed PMID: 18629538; PubMed Central PMCID:
Ananth CV, Peltier MR, Kinzler WL, Smulian JC, Vintzileos AM. Chronic
hypertension and risk of placental abruption: is the association modified by
ischemic placental disease? Am J Obstet Gynecol. 2007 Sep;197(3):273.e1-7. PubMed
Ananth CV, Peltier MR, Getahun D, Kirby RS, Vintzileos AM. Primiparity: an
‘intermediate’ risk group for spontaneous and medically indicated preterm birth.
J Matern Fetal Neonatal Med. 2007 Aug;20(8):605-11. PubMed PMID: 17674278.
Ananth CV, Peltier MR, Chavez MR, Kirby RS, Getahun D, Vintzileos AM.
Recurrence of ischemic placental disease. Obstet Gynecol. 2007 Jul;110(1):128-33.
PubMed PMID: 17601907.
Peltier MR, Ananth CV. Is the association of maternal smoking and
pregnancy-induced hypertension dependent on fetal growth? Am J Obstet Gynecol.
2007 Jun;196(6):532.e1-6. PubMed PMID: 17547883.
Peltier MR, Freeman AJ, Mu HH, Cole BC. Characterization of the
macrophage-stimulating activity from Ureaplasma urealyticum. Am J Reprod Immunol.
2007 Mar;57(3):186-92. PubMed PMID: 17295897.
Peltier MR, Barney BM, Brown MB. Effect of experimental genital mycoplasmosis
on production of matrix metalloproteinases in membranes and amniotic fluid of
Sprague-Dawley rats. Am J Reprod Immunol. 2007 Feb;57(2):116-21. PubMed PMID:
Peltier MR, Freeman AJ, Mu HH, Cole BC. Characterization and partial
purification of a macrophage-stimulating factor from Mycoplasma hominis. Am J
Reprod Immunol. 2005 Dec;54(6):342-51. PubMed PMID: 16305659.
Cole BC, Mu HH, Pennock ND, Hasebe A, Chan FV, Washburn LR, Peltier MR.
Isolation and partial purification of macrophage- and dendritic cell-activating
components from Mycoplasma arthritidis: association with organism virulence and
involvement with Toll-like receptor 2. Infect Immun. 2005 Sep;73(9):6039-47.
PubMed PMID: 16113324; PubMed Central PMCID: PMC1231055.
Esplin MS, Fausett MB, Peltier MR, Hamblin S, Silver RM, Branch DW, Adashi
EY, Whiting D. The use of cDNA microarray to identify differentially expressed
labor-associated genes within the human myometrium during labor. Am J Obstet
Gynecol. 2005 Aug;193(2):404-13. PubMed PMID: 16098862.
Esplin MS, Peltier MR, Hamblin S, Smith S, Fausett MB, Dildy GA, Branch DW,
Silver RM, Adashi EY. Monocyte chemotactic protein-1 expression is increased in
human gestational tissues during term and preterm labor. Placenta. 2005
Sep-Oct;26(8-9):661-71. Epub 2004 Dec 8. PubMed PMID: 16085045.
Peltier MR, Brown MB. Experimental genital mycoplasmosis causes increased
levels of mRNA for IL-6 and TNF-alpha in the placenta. Am J Reprod Immunol. 2005
Apr;53(4):189-98. PubMed PMID: 15760380.
Peltier MR. Immunology of term and preterm labor. Reprod Biol Endocrinol.
2003 Dec 2;1:122. Review. PubMed PMID: 14651749; PubMed Central PMCID: PMC305338.
Peltier MR, Richey LJ, Brown MB. Placental lesions caused by experimental
infection of Sprague-Dawley rats with Mycoplasma pulmonis. Am J Reprod Immunol.
2003 Sep;50(3):254-62. PubMed PMID: 14629031.