Eugene Chang

Eugene Chang

Associate Professor, Otolaryngology
Vice Chair, Academic Affairs - Otolaryngology
Associate Professor, Clinical Translational Sciences
Associate Professor, Neurosurgery
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Primary Department
Department Affiliations
(520) 626-6673

Research Interest

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.


Calton, J. B., Koripella, P. C., Willis, A. L., Le, C. H., Chiu, A. G., & Chang, E. H. (2016). Paranasal sinus size is decreased in CFTR heterozygotes with chronic rhinosinusitis. International forum of allergy & rhinology.

Cystic fibrosis (CF) heterozygotes with a single mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene are at significantly higher risk to develop chronic rhinosinusitis (CRS). However the reasons why remain unknown. We tested the hypothesis that CFTR heterozygotes would have smaller sinus volumes than healthy controls. To exclude sinus disease as a confounding factor we also assessed paranasal sinus volume in those with CRS, but without known CFTR mutations.

Carr, T. F., Hill, J. L., Chiu, A., & Chang, E. H. (2015). Alteration in Bacterial Culture After Treatment With Topical Mupirocin for Recalcitrant Chronic Rhinosinusitis. JAMA otolaryngology-- head & neck surgery, 1-5.

Topical mupirocin therapy is used to treat symptomatic chronic sinusitis (CRS). However, the potential adverse impact of this therapy on the sinus microbiota has not been well quantified.

Lee, M. H., Qu, Z., Fishbein, G. A., Lamp, S. T., Chang, E. H., Ohara, T., Voroshilovsky, O., Kil, J. R., Hamzei, A. R., Wang, N. C., Lin, S. F., Weiss, J. N., Garfinkel, A., Karagueuzian, H. S., & Chen, P. S. (2001). Patterns of wave break during ventricular fibrillation in isolated swine right ventricle. American journal of physiology. Heart and circulatory physiology, 281(1), H253-65.

Several different patterns of wave break have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. To determine the mechanism by which wave breaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in six isolated swine right ventricles (RV). Among 763 episodes of wave break (0.75 times x s(-1) x cm(-2)), optical maps showed three patterns: 80% due to a wave front encountering the refractory wave back of another wave, 11.5% due to wave fronts passing perpendicular to each other, and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in three-dimensional tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-tail interactions and filament break. We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wave break are produced by two fundamental mechanisms: head-tail interaction between waves and filament break.

Christensen, D. N., Franks, Z. G., McCrary, H. C., Saleh, A. A., & Chang, E. (2017). A systematic review of the association between cigarette smoke exposure and chronic rhinosinusitis. Otolaryngology-Head and Neck Surgery.
Le, C., McCrary, H. C., & Chang, E. (2016). Cystic Fibrosis Sinusitis. Advances in oto-rhino-laryngology, 79, 29-37.

Cystic fibrosis (CF) is an autosomal recessive genetic disorder caused by mutations in the CF transmembrane conductance regulator gene(CFTR) resulting in impaired ion transport. Nearly all people with CF will develop chronic rhino-sinusitis (CRS) and present with the characteristic viscous mucus, impaired mucociliary clearance and chronic inflammation/infection of the sinonasal cavity. While some individuals with CF can appear relatively asymptomatic in terms of their sinus disease, commonly reported symptoms include anosmia, headache, facial pain, nasal obstruction, chronic congestion and nasal discharge. Nasal endoscopy typically reveals mucosal edema, purulent discharge and nasal polyposis. Computed tomography (CT) imaging classically demonstrates the distinguishing findings of sinus hypoplasia or aplasia with generalized opacification, medial bulging of the lateral sinonasal sidewall and a demineralized uncinate process. Current treatment for CF sinusitis includes the use of hypertonic saline, topical and systemic steroids, antibiotics and endoscopic surgery. Research investigating novel therapies designed at targeting the primary defect of CF is showing promise for reversal of CF sinus disease, in addition to potential for disease prevention.