Heidi Mansour
Associate Professor, BIO5 Institute
Associate Professor, Clinical Translational Sciences
Associate Professor, Medicine
Associate Professor, Pharmaceutical Sciences
Primary Department
(520) 626-2768
Research Interest
Dr. Heidi M. Mansour, Ph.D., R.Ph. is a Tenured Associate Professor of Pharmaceutical Sciences in the College of Pharmacy with joint faculty appointments in the BIO5 Research Institute, the Clinical Translational Sciences graduate program in the UAHS, and the College of Medicine in the Division of Translational and Regenerative Medicine at The University of Arizona (UA) in Tucson, Arizona (USA). Dr. Mansour has a faculty member affiliation in the UA Institute of the Environment and is a research member the UA NCI Comprehensive Cancer Center Therapeutic Development Program. Dr. Mansour is Director of Pharmaceutics and Pharmacokinetics and Director of the Pharm.D./Ph.D. Dual Degree Program. She lectures in the B.S. Pharmaceutical Sciences undergraduate program, the Pharm.D. professional program and in the Pharmaceutics and Pharmacokinetics track of the graduate program at The University of Arizona. In addition to teaching, Dr. Mansour serves as Faculty Advisor in the Pharm.D./Ph.D. Dual-Degree Joint Program and Director of the Pharmaceutics and Pharmacokinetics track in the Pharmaceutical Sciences graduate program in The UA College of Pharmacy. As PI on multiple NIH, NSF, FDA, and pharmaceutical industrial grants, Dr. Mansour successfully leads multiple cutting-edge research projects. Her innovative research program has produced Assistant Professors who are employed at major research universities in the United States and in the Republic of S. Korea. In addition, her research program has produced Senior Research Scientists who are employed in major pharmaceutical companies in the United States. As Postdoc Mentor, Dr. Mansour has successfully mentored and trained over 10 Postdoctoral Research Scholars in my research program. As Major Professor, Dr. Mansour has successfully trained and graduated 3 doctoral graduate students with PhD degrees. Her mentoring experience extends as an active faculty mentor in the ATS Assembly Mentorship Program for several mentees in the ATS Assemblies each year. Dr. Mansour has published over 80 peer-reviewed scientific journal papers, 13 book chapters, 2 edited books, and over 100 scientific conference abstracts. She serves on the Editorial Advisory Boards of the The Royal Society of Chemistry Molecular Systems Design & Engineering, APhA/FIP Journal of Pharmaceutical Sciences, and Pharmaceutical Technology. Research in the Mansour GLP-approved labs focuses on the design, development, and optimization of advanced drug delivery systems and drug dosage forms. A systematic Quality-by-Design (QbD) approach includes in silico computational molecular modeling for predictive drug and formulation modeling, comprehensive physicocharacterization, advanced microscopy imaging, design of experiments (DOEs), formulation, USP/FDA-required in vitro performance studies, in vitro cellular studies, in vivo rodent animal studies for pharmacokinetics/pharmacodynamics/drug biodistribution, and translation medicine experiments. Dr. Mansour is an annual Faculty Instructor at ISAM (International Society of Aerosols in Medicine) Aerosol School, instructor in two online webinars on inhalation aerosol drug delivery, and instructor in Buchi Advanced Spray Drying short-courses. She was recently Co-Chair of the Drug Delivery: New Devices & Emerging Therapies Group in the International Society of Aerosols in Medicine (ISAM), and has been an expert member of NIH NICHD U.S. Pediatric Formulations Initiative New Drug Delivery Systems Aerosols Working Group for several years. Dr. Mansour currently serves on the Drug/Device Discovery and Development (DDDD) Committee of the American Thoracic Society (ATS). She regularly serves as an expert reviewer for scientific journals and grant funding agencies including NIH study sections, Department of Defense (DOD) study panels, National Science Foundation (NSF) study panels, AAAS, Catalent Drug Delivery Institute and international funding agencies such as the German-Israeli Foundation, German International Exchange Service (DAAD), Cochrane Airways Group of the National Health Service (London, England), Engineering and Physical Sciences Research Council (London, England), PRESTIGE Postdoc Fellowship Programme of the European Commission (Paris, France), and the Biomedical Innovation Program of the French National Research Agency (Paris, France). In addition to serving on NSF study panels, NIH study sections, and international study panels in the European Union and Great Britain, her innovative research program continuously attracts competitive funding awards from federal sources (NIH, NSF, FDA, DOD) and the pharmaceutical industry. In addition to lecturing in the BS Pharmaceutical Sciences undergraduate, Ph.D. graduate, and Pharm.D. professional programs, Dr. Mansour leads her research labs where she trains postdoctoral scholars, visiting scholars, visiting professors, graduate students, Pharm.D. student researchers, and physician-scientist (MD/PhD) fellows. As Major Professor and mentor, her research program has successfully graduated several Ph.D.s. Her innovative research program has produced Assistant Professors employed at research universities in the United States and in the Republic of S. Korea and Senior Research Scientists employed at major pharmaceutical companies in the United States. Dr. Mansour is an active, long-time member of several scientific organizations and elected member to honor societies, including the Sigma Xi Scientific Research Honor Society, Rho Chi Pharmaceutical Honor Society, and Golden Key International Honor Society. As a registered pharmacist for over 20 years, she earned her BS in pharmacy with honors and distinction, a PhD minor in advanced physical and interfacial chemistry (Department of Chemistry), and a PhD major in drug delivery/pharmaceutics (School of Pharmacy) from the University of Wisconsin-Madison. Also at the U.W.-Madison, she had been a Clinical Instructor for a few years. Having completed postdoctoral fellowships at the U.W.-Madison and at the University of North Carolina-Chapel Hill, she was awarded the UNC-Chapel Hill Postdoctoral Award for Research Excellence from the Office of the Vice-Chancellor, the AAPS Postdoctoral Fellow Award in Research Excellence, and the PhRMA Foundation Postdoctoral Fellowship award. As an Instructor, she served on the Graduate Faculty at UNC-Chapel Hill.


de la Vega, M. R., Dodson, M., Gross, C., Manzour, H., Lantz, R. C., Chapman, E., Wang, T., Black, S. M., Garcia, J. G., & Zhang, D. D. (2016). Role of Nrf2 and Autophagy in Acute Lung Injury. Current pharmacology reports, 2(2), 91-101.
BIO5 Collaborators
Clark Lantz, Heidi Mansour

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the clinical manifestations of severe lung damage and respiratory failure. Characterized by severe inflammation and compromised lung function, ALI/ARDS result in very high mortality of affected individuals. Currently, there are no effective treatments for ALI/ARDS, and ironically, therapies intended to aid patients (specifically mechanical ventilation, MV) may aggravate the symptoms. Key events contributing to the development of ALI/ARDS are: increased oxidative and proteotoxic stresses, unresolved inflammation, and compromised alveolar-capillary barrier function. Since the airways and lung tissues are constantly exposed to gaseous oxygen and airborne toxicants, the bronchial and alveolar epithelial cells are under higher oxidative stress than other tissues. Cellular protection against oxidative stress and xenobiotics is mainly conferred by Nrf2, a transcription factor that promotes the expression of genes that regulate oxidative stress, xenobiotic metabolism and excretion, inflammation, apoptosis, autophagy, and cellular bioenergetics. Numerous studies have demonstrated the importance of Nrf2 activation in the protection against ALI/ARDS, as pharmacological activation of Nrf2 prevents the occurrence or mitigates the severity of ALI/ARDS. Another promising new therapeutic strategy in the prevention and treatment of ALI/ARDS is the activation of autophagy, a bulk protein and organelle degradation pathway. In this review, we will discuss the strategy of concerted activation of Nrf2 and autophagy as a preventive and therapeutic intervention to ameliorate ALI/ARDS.

Willis, L., Hayes Jr., D., & Mansour, H. M. (2012). Therapeutic liposomal dry powder inhalation aerosols for targeted lung delivery. Lung (Impact Factor: 2.171), 190(3), 251-262.

PMID: 22274758;Abstract:

Therapeutic liposomal powders (i.e., lipospheres and proliposomes) for dry powder inhalation aerosol delivery, formulated with phospholipids similar to endogenous lung surfactant, offer unique opportunities in pulmonary nanomedicine while offering controlled release and enhanced stability. Many pulmonary diseases such as lung cancer, tuberculosis (TB), cystic fibrosis (CF), bacterial and fungal lung infections, asthma, and chronic obstructive pulmonary disease (COPD) could greatly benefit from this type of pulmonary nanomedicine approach that can be delivered in a targeted manner by dry powder inhalers (DPIs). These delivery systems may require smaller doses for efficacy, exhibit reduced toxicity, fewer side effects, controlled drug release over a prolonged time period, and increased formulation stability as inhaled powders. This state-of-the-art review presents these novel aspects in depth. © Springer Science+Business Media, LLC 2012.

Hayes Jr., D., Baker, P. B., Mansour, H. M., Peeples, M. E., & Nicol, K. K. (2013). Interstitial lung disease in a child with antisynthetase syndrome. Lung (Impact Factor: 2.171), 191(4), 441-443.

PMID: 23652349;Abstract:

Introduction: Antisynthetase Syndrome is associated with interstitial lung disease in adult patients, but this has not been described in children. Materials and methods: A 13-year-old with interstitial lung disease due to Antisynthetase Syndrome and pulmonary arterial hypertension underwent emergent bilateral lung transplantation after a rapid clinical decline. Conclusion: We present the clinical, radiographic, and histological findings of a child with interstitial lung disease due to Antisynthetase Syndrome. © 2013 Springer Science+Business Media New York.

Hayes Jr., D., & Mansour, H. M. (2012). Vanishing bronchus intermedius syndrome in a pediatric patient with cystic fibrosis after lung transplantation. Pediatric Transplantation (Impact Factor: 1.630), 16(8), E333-E337.

PMID: 22489792;Abstract:

Airway complications occur frequently after lung transplantation. Bronchial stenosis is the most frequently encountered complication with the most severe form of that being the vanishing bronchus intermedius syndrome (VBIS). This rare disorder has never been reported in the pediatric population. This is the first report of VBIS in a pediatric patient, specifically a 16-yr-old male patient with cystic fibrosis whose course was complicated by a lower airway infection with Aspergillus fumigatus. The VBIS responded to bronchoscopic balloon dilation and placement of an airway stent. © 2012 John Wiley & Sons A/S.

Mansour, H. M., & Zografi, G. (2007). Relationships between equilibrium spreading pressure and phase equilibria of phospholipid bilayers and monolayers at the air-water interface. Langmuir (Impact Factor: 4.384), 23(7), 3809-3819.

PMID: 17323986;Abstract:

The intricate interplay between the bilayer and monolayer properties of phosphatidylcholine (PC), phosphatidylglycerol (PG), and phosphatidylethanolamine (PE) phospholipids, in relation to their polar headgroup properties, and the effects of chain permutations on those polar headgroup properties have been demonstrated for the first time with a set of time-independent bilayer-monolayer equilibria studies. Bilayer and monolayer phase behavior for PE is quite different than that observed for PC and PG. This difference is attributed to the characteristic biophysical PE polar headgroup property of favorable intermolecular hydrogen-bonding and electrostatic interactions in both the bilayer and monolayer states, This characteristic hydrogen-bonding ability of the PE polar headgroup is reflected in the condensed nature of PE monolayers and a decrease in equilibrium monolayer collapse pressure at temperatures below the monolayer critical temperature, Tc (whether above or below the monolayer triple point temperature, Tc. This interesting phenomena is compared to equilibrated PC and PG monolayers which collapse to form bilayers at 45 mN/m at temperatures both above and below monolayer Tc. Additionally, it has been demonstrated by measurements of the equilibrium spreading pressure, πe, that at temperatures above the bilayer main gel-to-liquid-crystalline phase-transition temperature, Tm, all liquid-crystalline phospholipid bilayers spread to form monolayers with πe, around 45 mN/m, and spread liquid-expanded equilibrated monolayers collapse at 45 mN/m to form their respective thermodynamically stable liquidcrystalline bilayers. At temperatures below bilayer Tm, PC and PG gel bilayers exhibit a drop in bilayer πe values ≤0.2 mN/m forming gaseous monolayers, whereas the value of ≤c of spread monolayers remains around 45 mN/m. This suggests that spread equilibrated PC and PG monolayers collapse to a metastable liquid-crystalline bilayer structure at temperatures below bilayer Tm (where the thermodynamically stable bilayer liquid-crystalline phase does not exist) and with a surface pressure of 45 mN/m, a surface chemical property characteristically observed at temperatures above bilayer Tm (monolayer Tc). In contrast, PE gel bilayers, which exist at temperatures below bilayer Tm but above bilayer Ts, (bilayer crystal-to-gel phase-transition temperature), exhibit gel bilayer spreading to form equilibrated monolayers with intermediate ≤e, values in the range of 30-40 mN/m; however, bilayer ne and monolayer ≤c values remain equal in value to one another. Contrastingly, at temperatures below bilayer Ts, PE crystalline bilayers exhibit bilayer ≤e, values ≤0.2 mN/m forming equilibrated gaseous monolayers, whereas spread monolayers collapse at a value of ≤c remaining around 30 mN/m, indicative of metastable gel bilayer formation. © 2007 American Chemical Society.