Neonatology

Amy T. Nathan, MD

Appointment

Research Instructor

Email

amy.nathan@cchmc.org

Phone

513-636-0282

Fax

513-636-5355

Bio

Lung injury continues to be a major cause of morbidity and mortality for premature infants, and evidence points to both inflammation and mechanical stress as important factors in exacerbating this injury. The reaction to environmental stimuli such as chorioamnionitis or mechanical ventilation varies between individuals, and may be related to their unique immune responses. Neonates are known to be biased towards allergic, or Th2-type responses. The balance between Th1 and Th2 effector cells determines the profile of cytokines that are released in response to various stimuli, and may detemine which children develop asthma or other atopic diseases.

Amy Nathan, MD, has an interest in studying the factors that influence the polarization of T helper cells, looking in particular at regulatory T cells which serve to inhibit effector T cells. The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) has been shown to impair T Cell proliferation and activation, and may serve to modulate the population of T cells in the lung. Dr. Nathan is invesitgating the effect of the Th2-biased cytokine interleukin-13 on IDO expression in the lung, and the subsequent balance between regulatory and effector T cells.

Dr. Nathan is a practicing neonatologist and attends at Good Samaritan Hospital. Her clinical intersts include ventilatory strategies for reducing lung injury as well as focusing on family-centerd care.

Credentials

MD: Yale University School of Medicine, 1998

Residency: Pediatrics, University of North Carolina, Chapel Hill, 1998-2001

Fellowship: Neonatology, University of North Carolina, Chapel Hill, 2002-2005

Certification: Pediatrics 2001

Awards and Honors

Research Merit Award for best basic science presentation, Thomas F. Boat Evening of Scholarship, University of North Carolina, 2003

House Officer Award, University of North Carolina Hospitals, 2005

Research

Asthmatic lung inflammation, especially influence of interleukin-13 on chemokine production, gene expression and asthmatic phenotype.

Research Grants and Contracts

University of North Carolina Medical Alumni Endowment Fund grant 7/2005-6/2005

Medimmune Research grant 7/2004-6/2005

Professional Organization Memberships

American Academy of Pediatrics

Perinatal Section of American Academy of Pediatrics

Special Interests

Lung injury and inflammation
Ventilation strategies to reduce lung injury

Recent Presentations / Invited Lectures

The Irritable Baby, 15th annual North Carolina Neonatal Nursing Institute, 2005, Chapel Hill, NC.

Neonatal Abstinence Syndrome, 12th Annual Perinatal/Neonatal RegionalUpdate, 2004, Wilmington, NC.

Effects of IL-13 on chemokine production by monocytes and respiratory epithelium, Thomas F. Boat Evening of Scholorship, University of North Carolina, 2004, Chapel Hill, NC.