Julie Ledford

Julie Ledford

Associate Professor, Cellular and Molecular Medicine
Associate Professor, Immunobiology
Associate Professor, Medicine
Associate Professor, Clinical Translational Sciences
Associate Professor, Applied BioSciences - GIDP
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Primary Department
Contact
(520) 626-0276

Work Summary

Julie Ledford's research focuses on respiratory disease, and genetic and molecular mechanisms of allergic airway diseases in children.

Research Interest

Dr. Ledford’s current work in the area of pulmonary surfactant immunobiology combines her knowledge of mouse genetics, pulmonary disease models and immune function regulation and focuses on understanding the role of Surfactant Protein-A (SP-A) and how it regulates signaling pathways within various immune cell populations. Specifically, she is interested in how SP-A regulates degranulation, either directly or indirectly, of two important cell types in asthma: mast cells and eosinophils. More recently, Dr. Ledford’s research has focused on understanding how genetic variation within human SP-A2 alters functionality of the protein in relation to eosinophil activities and how this translates to characteristics observed in human asthma.

Publications

Ledford, J., Wang, Y., Francisco, D., Manne, A., Addison, K., Billheimer, D., Chu, H. W., Voelker, D., & Kraft, M. (2017). Genetic Variation in Surfactant Protein-A2 Results in Heightened Responses to IL-13 and Reduced Lung Function in Asthmatics. Science Translational Medicine.
Ledford, J. G., Goto, H., Potts, E. N., Degan, S., Wei Chu, H., Voelker, D. R., Sunday, M. E., Cianciolo, G. J., Foster, W. M., Kraft, M., & Wright, J. R. (2015). Correction: SP-A Preserves Airway Homeostasis during Mycoplasma pneumoniae Infection in Mice. Journal of immunology (Baltimore, Md. : 1950), 195(6), 2917-8.
Ledford, J. G., Kovarova, M., Jania, L. A., Nguyen, M., & Koller, B. H. (2012). ONZIN deficiency attenuates contact hypersensitivity responses in mice. Immunology and cell biology, 90(7), 733-42.

ONZIN is abundantly expressed in immune cells of both the myeloid and lymphoid lineage. Expression by lymphoid cells has been reported to further increase after cutaneous exposure of mice to antigens and haptens capable of inducing contact hypersensitivity (CHS), suggesting that ONZIN has a critical role in this response. Here, we report that indeed ONZIN-deficient mice develop attenuated CHS to a number of different haptens. Dampened CHS responses correlated with a significant reduction in pro-inflammatory IL-6 at the challenge site in ONZIN-deficient animals, compared with wild-type controls. Together the study of these animals indicates that loss of ONZIN impacts the effector phase of the CHS response through the regulation of pro-inflammatory factors.

Goto, H., Ledford, J. G., Mukherjee, S., Noble, P. W., Williams, K. L., & Wright, J. R. (2010). The role of surfactant protein A in bleomycin-induced acute lung injury. American journal of respiratory and critical care medicine, 181(12), 1336-44.

Surfactant protein A (SP-A) is a collectin family member that has multiple immunomodulatory roles in lung host defense. SP-A levels are altered in the bronchoalveolar lavage (BAL) fluid and serum of patients with acute lung injury and acute respiratory distress syndrome, suggesting the importance of SP-A in the pathogenesis of acute lung injury.

Lugogo, N., Francisco, D., Addison, K. J., Manne, A., Pederson, W., Ingram, J. L., Green, C. L., Suratt, B. T., Lee, J. J., Sunday, M. E., Kraft, M., & Ledford, J. G. (2017). Obese asthmatic patients have decreased surfactant protein A levels: Mechanisms and implications. The Journal of allergy and clinical immunology.

Eosinophils are prominent in some patients with asthma and are increased in the submucosa in a subgroup of obese patients with asthma (OAs). Surfactant protein A (SP-A) modulates host responses to infectious and environmental insults.