A2DRC Research Update Seminar with Dr. Julie Ledford

The Asthma & Airway Disease Research Center at the University of Arizona Health Sciences Campus Presents:

Research Update Seminar Series

Thursday, Nov. 29, 2018
4 - 5 p.m.
UA College of Medicine - Tucson
Conference Room 2343

“CC16: A Link between Airway Infection and Obstructive Lung Disease?”

Presented by:

Julie Ledford, PhD
Assistant Professor of Medicine
Assistant Professor of Immunobiology
University of Arizona/ BIO5 Institute

Dr. Ledford is an assistant professor of medicine and immunobiology at the University of Arizona and is an active member of the UAHS Asthma & Airway Disease Research Center, the UA BIO5 Institute, the Southwest Environmental Health Sciences Center and has faculty appointments in the Graduate Interdisciplinary Program in the Physiological Sciences and in the Allergy and Immunology Fellowship Training program. She received her doctoral training in genetics and molecular biology at the University of North Carolina at Chapel Hill and completed her postdoctoral training in surfactant immunobiology at Duke University.

Dr. Ledford’s research interests are centered around pulmonary proteins that are secreted and reside within the air-lung interface and mediate immunity to inhaled pathogens and allergens. Of particular interest are two proteins, which are among the most highly expressed pulmonary proteins in humans: surfactant protein-A (SP-A) and club cell secretory protein (CCSP). Working closely with clinical translational collaborators, her research team has discovered that some asthmatics express a genetic variant in SP-A that renders them more likely to have lower lung function, worse asthma control and higher levels of peripheral eosinophils. Based on these findings, her current research is focused on drug development with an SP-A 10 AA peptide that can rescue the activity of the dysfunctional SP-A allele.

Additionally, Dr. Ledford’s research group has discovered that obese asthmatics have less SP-A in their lungs, which may contribute to a decreased ability to clear eosinophils from the lung tissue. Working with a team of clinicians and basic scientists, they are exploring mechanisms by which obese asthmatics would have less SP-A as compared to lean asthmatics, which may be a consequence of a heightened cytokine milieu coupled with increased chest wall pressure.

Please join us!

Contact: Eva Barrow, evachere@email.arizona.edu