Skip to main content
Associate Professor, BIO5 Institute
Associate Professor, Clinical Translational Sciences
Associate Professor, Neurosurgery
Associate Professor, Otolaryngology
Vice Chair, Academic Affairs - Otolaryngology
Dr. Chang’s research is divided into three areas.Cystic fibrosis (CF) research: Dr. Chang is investigating the role of the cystic fibrosis transmembrane conductance regulator (CFTR) gene in the pathogenesis of chronic sinusitis. He published the first animal model of CF sinus disease, and has characterized novel therapies including gene therapy vectors and CFTR potentiators in improving CF sinus disease in both animals and humans.Sinus microbiome research: the “microbiome” is the microbial community that is present in the human body. The sinonasal cavities have traditionally been thought to be sterile cavities, but new research is beginning to elucidate the vast number of microbial communities that populate our sinus. With this knowledge, we are investigating how our current therapies can influence this microbial population and prevent sinus disease.Impact of the upper and lower airway: as otolaryngologists, our focus has been in the airway of the head and neck. Dr. Chang has been investigating how the upper airway can influence disease of the lower airway, and vice versa. This research can influence the understanding of common diseases of the lower airway, such as asthma and chronic obstructive pulmonary disease (COPD).Dr. Chang receives active funding research support from the NIH, and the Cystic Fibrosis Foundation.
Barry, J. Y., Le, C. H., Baumann, J., Skinker, L., Chiu, A. G., & Chang, E. (2016). Endoscopic resection of maxillary sinus keratocystic odontogenic tumors. Laryngoscope. doi:10.1002/lary.25920
Potter, N. J., Graham, S. M., Chang, E., & Greenlee, J. D. (2015). Bioabsorbable plate cranial base reconstruction. Laryngoscope. doi:10.1002/lary.24991
Noutsios, G. T., Willis, A. L., Ledford, J. G., & Chang, E. (2017). Novel role of surfactant protein A in bacterial sinusitis. Int Forum Allergy Rhinol.
Eugene Chang, Julie Ledford
Dlouhy, B. J., Madhavan, K., Clinger, J. D., Reddy, A., Dawson, J. D., O'Brien, E. K., Chang, E., Graham, S. M., & Greenlee, J. D. (2012). Elevated body mass index and risk of postoperative CSF leak following transsphenoidal surgery. Journal of neurosurgery, 116(6), 1311-7.
Postoperative CSF leakage can be a serious complication after a transsphenoidal surgical approach. An elevated body mass index (BMI) is a significant risk factor for spontaneous CSF leaks. However, there is no evidence correlating BMI with postoperative CSF leak after transsphenoidal surgery. The authors hypothesized that patients with elevated BMI would have a higher incidence of CSF leakage complications following transsphenoidal surgery.
Chang, E. H., Lacruz, R. S., Bromage, T. G., Bringas, P., Welsh, M. J., Zabner, J., & Paine, M. L. (2011). Enamel pathology resulting from loss of function in the cystic fibrosis transmembrane conductance regulator in a porcine animal model. Cells, tissues, organs, 194(2-4), 249-54.
Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR), a phosphorylation- and ATP-regulated anion channel. CFTR expression and activity is frequently associated with an anion exchanger (AE) such as AE2 coded by the Slc4a2 gene. Mice null for Cftr and mice null for Slc4a2 have enamel defects, and there are some case reports of enamel anomalies in patients with CF. In this study we demonstrate that both Cftr and AE2 expression increased significantly during the rat enamel maturation stage versus the earlier secretory stage (5.6- and 2.9-fold, respectively). These qPCR data im- ply that there is a greater demand for Cl(-) and bicarbonate (HCO₃⁻) transport during the maturation stage of enamel formation, and that this is, at least in part, provided by changes in Cftr and AE2 expression. In addition, the enamel phenotypes of 2 porcine models of CF, CFTR-null, and CFTR-ΔF508 have been examined using backscattered electron microscopy in a scanning electron microscope. The enamel of newborn CFTR-null and CFTR-ΔF508 animals is hypomineralized. Together, these data provide a molecular basis for interpreting enamel disease associated with disruptions to CFTR and AE2 expression.