Roles
Professor
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Biography
Dr. Wanner is the Joseph Weintraub Professor of Medicine at the University of Miami Miller School of Medicine.
Throughout his research career, he has been interested in airway biology, especially the regulation of airway secretions and their clearance from the airways. However, Dr. Wanner’s more recent work has focused on novel interactions between commonly used airway medications in the treatment of asthma and COPD, especially with respect to the drugs’ bronchodilator and anti-inflammatory actions. Over
Dr. Wanner has published 270 original research papers and has written 55 book chapters. He continues to be active in the laboratory where he interacts with other independent investigators and mentors research fellows and junior faculty.
Long active in the American Thoracic Society, Dr. Wanner was President of ATS in 2001-2002. He has been active on a number of editorial boards, and has served on and chaired several NIH study sections. He has chaired the VA Merit Review Board for Pulmonary Diseases and had uninterrupted federal grant support for over 30 years in the past. He has served as Scientific Director of the Alpha-1 Foundation. -
Education & Training
Education
Post Graduate Training
Licensures and Certifications
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Honors & Awards
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Teaching Interests
I have been teaching medical students, residents and fellows since 1972. As Division Chief of the Pulmonary Division at UM from 1983 to 2005, I was involved in the organization of the fellowship program. I have participated in the BME 501 Unified Medical Sciences Course (respiratory system), the Sophomore Mechanism of Disease Course and the Sophomore Pharmacology Course. -
Research Interests
Airway mucociliary transport involves the interaction among ciliary activity and airway surface liquid, the product of surface epithelial water flux and mucus secreted by mucus glands. This ensures the physical clearance of material trapped in the surface liquid. In addition, the biochemical constituents of airway secretions (ant-oxidants and antimicrobial molecules) contribute to airway host defenses. The regulation of ciliary activity and secretory function were investigated in vitro and in vivo. Our studies showed that allergic airway inflammation in sheep, human asthma and COPD are associated with impaired mucociliary clearance due to changes in ciliary activity as well as the quantity and biochemical composition of mucus, that increased inhaled oxygen concentrations, volatile atmospheric pollutants and cigarette smoking impair mucociliary clearance, and that beta-adrenergic agonists are mucociliary stimulants. These investigations were supported by NIH HL18356 - Structure and Function in Intact Human Airways (PI), NIH HL20989 - Pathophysiology of Bronchial Asthma (PI), NIH ESO3041 - Pathogenesis of Pollutant Induced Mucociliary Dysfunction in the Airways (PI), NIH HL31722 - Defense Functions in the Developing Respiratory System (PI), NIH NRSA HL07578 - Training Grant in Pulmonary Disease (PD), NIH HL33897 - Mechanisms of Late Phase Pulmonary Responses (Co-I).
Our studies have shown that the response of airway blood flow to inhaled beta-adrenergic agonists is blunted in asthma, healthy smokers and patients with COPD, and that beta-adrenergic responsiveness can be restored by inhaled corticosteroids. In other words, these conditions are associated with reversible endothelial dysfunction in the airway circulation. We also made the novel observation that glucocorticoids acutely potentiate b2-adrenergic agonist-induced vasodilation in the airway, due to a non-genomic interaction involving the local disposal of the beta-adrenergic agonist. Airway vascular smooth muscle cells express the organic cationic transporter OCT3. OCT3 is inhibited by glucocorticoids, an acute action not involving gene transcription and translation. The inhibition of OCT3 function by glucocorticoids prevents the entry of hydrophilic b2-adrenergic agonist into vascular smooth muscle cells (containing intracellular catechol-disposing enzymes) thereby increasing the concentration of b2-adrenergic agonists at b2-adrenergic receptor sites and potentiating vascular smooth muscle relaxation. These investigations were supported by NIH NIAID HL58086 - Alpha-Adrenergic Regulation of Airway Blood Flow (PI) and 23 academic grants from industry. -
Publications
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Professional Activities
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