Dr. Nazeeh Hanna has been a faculty member and Chief of Neonatology at Winthrop University Hospital since 2007. He is currently an Associate Professor of Pediatrics, State University of New York at Stony Brook. Following his medical education from Ain-Shams University in Egypt, he received his Pediatric training at Albany Medical Center and his Neonatal fellowship training at Brown University. Before joining Winthrop University Hospital, Dr. Hanna was Associate Professor of Pediatrics and the Co-Chief of Neonatology at UMDNJ-Robert Wood Johnson Medical School. Dr. Hanna is an established investigator who has international recognition for his work in reproductive immunology. His research track is focused in the area of developmental immunology and the potential impact of maternal exposure to environmental toxicants on preterm births. Dr. Hanna research interests were funded by several national agencies including NIH, NICHD, American Lung Association and National Institute of Environmental Health Sciences. Dr. Hanna has been an invited speaker or a Chair in National conferences on Neonatology and Reproductive Biology/Immunology. He is currently a member of several professional organizations including the American Academy of Pediatrics, Society for Pediatrics Research, American Pediatric Society, American Medical Association, Eastern Society for Pediatrics Research and American Society of Reproductive Immunology. He was selected as a member for the American Diabetes Association (ADA) Research Grant Review Committee as well ad hoc reviewer for several NIH study sections. Dr. Hanna serves on the Editorial Board of American Journal of Reproductive Immunology. In addition, he is a regular reviewer for several prestigious journals.
Description of Research Interests/Activities
Infants born prematurely are at increased risk of early postnatal and later developmental problems. Approximately 25% of premature babies less than 25 weeks have severe disabilities. Very premature infants who do not have severe disabilities are nevertheless at increased risk for cognitive, perceptual and behavioral problems. With advances in prenatal and neonatal care, there has been improvement in survival, but improvements in function and outcome have lagged. The optimal way to reduce complications of prematurity is to reduce the incidence of prematurity itself.
Dr. Hanna’s research interest focuses on evaluating altered immune function in pregnancy and preterm labor and the potential impact of maternal exposure to environmental toxicants on this disorder. The results of these studies will help bridge the gap between clinical and basic research and set the stage for future collaborative interdisciplinary studies. Dr. Hanna’s work elucidates the role of cytokines in fetal immune defense, namely interleukin-10 (IL-10) which is an anti-inflammatory agent produced by the placenta and plays an important role in the maintenance of normal pregnancy. IL-10 will counteract the harmful functions of the maternal immune cells, hence protecting the fetus. The overall hypothesis is that premature withdrawal of immunoregulatory molecules such as IL-10 will allow for increased expression of parturition inducing pro-inflammatory mediators and collagen degrading matrix metalloproteinases that may lead to preterm labor.
Dr. Hanna is currently directing several ongoing studies including characterization of the molecular mechanisms signaling IL-10 expression in gestational tissues, understanding the role of progesterone and prostaglandins in regulating the production of placenta cytokines, investigating the role of COX-2 inhibitors in preventing preterm labor, as well as elucidating environmental toxins-linked mechanisms of preterm labor. Dr. Hanna was recently awarded NIH grant titled: New Model Leading to Preterm Delivery: Role of Exposure to Environmental Toxins. The major goal of this project is to explore the interactions between inflammation and environmental toxins in preterm birth. In addition, using specific methodology, Dr. Hanna recently identified specific set of cytokines present in cervical secretions during pregnancy that help monitoring intrauterine inflammatory milieu in pregnancy. This methodology provides an easy, non-invasive way to monitor and understand intracervical immunity and its contribution to certain perinatal disease processes such as prematurity, intrauterine growth restriction, recurrent pregnancy loss, and preeclampsia.
The studies done at Winthrop University Hospital will contribute significantly to our understanding of the molecular pathogenesis of preterm labor and the role of exposure to environmental toxicants on this pathologic process. This work is exciting because it provides a novel model on the pathogenesis of preterm labor. As our understanding of mechanisms behind preterm labor and the role of inflammation grows, Dr. Hanna’s findings may ultimately suggest new strategies to predict, treat or prevent preterm labor.
Areas of Experience
Research Team Members
Please see attached: Women and Children Research Institute.
Clinical Practice and Interests
N. Hanna, I. Hanna, E. Wagner, M. Hleb, D. Balkundi and S. Sharma. Gestational Age-dependent Expression of Interleukin-10 and its receptor in Human Placental Tissues and isolated Cytotrophoblasts. J. Immunol.164:5721-5728, 2000.
E. Wagner, N. Hanna, L. Fast, N. Kouttab, P. Shank, A. Vasquez and S. Sharma. Novel Diversity in IL-4-Mediated Responses in Resting Human Naive B Cells versus Germinal Center/Memory B Cells. J. Immunol.165:5573-9. 2000.
M. Plaveyak, N. Hanna, C. Erckefelt, M. Leif and S. Sharma. Deficiency of decidual IL-10 in first trimester missed abortions: A lack of correlation with decidual immune cell profile. Am. J. Reprod. Immunol. 47:242-250 April 2002
A. Petrova, N. Hanna, R. Mehta. Gestational age related maternal fetal Neonatal Humoral Immunity. J. Appl. Res. Vol. 4, No. 1, March 2004
N. Hanna, L. Bonifacio, P. Reddy, I. Hanna, B. Weinberger, S. Murphy, D. Laskin, S. Sharma: IFN-?-Mediated Inhibition of COX-2 Expression in the Placenta from Term and Preterm Labor Pregnancies Am J Reprod Immunol. 2004 Apr;51:311-3118.
M. Hleb, S. Murphy, E. Wagner, N. Hanna, N. Sharma, J. Park, X. Li, T. Strom, J. Padbury, and S. Sharma. Evidence for cyclin D3 as a novel target of rapamycin in human T lymphocytes
J. Biol. Chem., May 2004; 10.1074
N. Hanna, P. Vasquez, T. Mariano, S. Gentile, C. DeCoste, D. Heck, J. Laskin, D. Laskin, B. Weinberger. Mechanisms Underlying Reduced Apoptosis in Neonatal Neutrophils. Pediatr Res. 2005 Jan;57(1):56-62.
S. Murphy, L. Fast, N. Hanna and S. Sharma. Uterine NK Cells Mediate Inflammation-Induced Fetal Demise in IL-10-Null Mice. J Immunol October, 2005 175: p. 4084-4090.
N. Hanna, L. Bonifacio, B. Weinberger, P. Reddy, S. Murphy, R. Romero, D. Laskin and S. Sharma. Evidence for IL-10-mediated Inhibition of Cyclooxygenase-2 (COX-2) Expression and Prostaglandin Production by Preterm Human Placenta. Am J Reprod Immunol. 2006 Jan;55(1):19-27
Weinberger B, Vetrano AM, Syed K, Murthy S, Hanna N, Laskin JD, Laskin DL. Influence of Labor on Neonatal Neutrophil Apoptosis, and Inflammatory Activity. Pediatr Res. 2007 Mar 15;
M. Mondestin-Sorrentino, J. Smulian, A. Vintzileos, C. Ananth, S. Sharma and N. Hanna. Variations in Cervical IL-10 and IL-8 Concentrations Throughout Gestation in Normal Pregnancies. Am J Reprod Immunol. 2007 Jun;57(6):482-487.
Murphy, S., Hanna, N.., Fast, L., Shaw, S.K., Berg, G., Padbury, G., Romero, R., and Sharma, S. Evidence for participation of uterine natural killer cells in the mechanisms responsible for spontaneous preterm labor and delivery. Am J Obstet Gynecol. 2009 Mar;200(3):308.e1-9.
Kiefer, D., Keeler, S., Rust, O., Wayock, C., Vintzileos, A. and Hanna, N. Is midtrimester short cervix a sign of intraamniotic inflammation? Am J Obstet Gynecol 2009;200:374.e1-374.e5.
Keeler, S., Kiefer, D., Rust, O., Vintzileos, A., Atlas, R., Bornstein, E. and Hanna, N. Comprehensive amniotic fluid cytokine profile evaluation in women with a short cervix: which cytokine(s) correlates best with outcome? Am J Obstet Gynecol 2009;201:276.e1-6.
Mehmet Bayraktar, Morgan Peltier, Anna Vetrano, Yuko Arita, Jeffrey Kazzaz, Surendra Sharma and Nazeeh Hanna. IL-10 can modulate placental responses to TLR ligands. Am J Reprod Immunol. 2009 Dec;62(6):390-9. Epub 2009 Oct 11.
Please see attached: Women and Children Research Institute.