Matthias A. Salathe, M.D.
- Office: 305-243-6388
- Fax: 305-243-6992
- Internal Medicine
- Pulmonary Disease - Internal Medicine
- Critical Care Medicine-Internal Medicine
Cystic Fibrosis, Bronchiectasis, Non-tuberculous Mycobacterial Lung Disease, COPD
- American Board of Internal Medicine
- American Board of Internal Med-Pulmonary Disease
- American Board of Internal Med-Critical Care Medicine
- Chief, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine
- Professor of Medicine and Molecular & Cellular Pharmacology
- Vice Chair for Research
Airway epithelial cell biology, including pathobiology of chronic bronchitis and cystic fibrosis
The Salathe lab has experience studying airway diseases, in particular signaling in airway epithelial cells. Towards this end, it was instrumental in developing programs and microscope setups to measure ciliary beat frequency (CBF) and fluorescent signals (including Ca2+, pH, and FRET for PKA activation) simultaneously in the same single, live cell. The lab also adapted measurements for ASL volume determination. Together with collaborators, the lab has helped to establish a biorepository of airway epithelial cells from now >500 lungs (organ donors) used for air-liquid interface (ALI) cultures and airway samples from patients with airway diseases (including BAL, brushed cells, exhaled breath condensate, and blood for other analyses including cytokines and genetics). The lab initiated the development of lentivirus-based manipulation of airway epithelial cell proteins to measure cAMP by FRET (using fluorescently tagged PKA subunit expression in ciliated cells, driven by the ciliated cell specific foxj1 promoter) and to suppress proteins for analysis of their role in signal transduction (e.g., pannexin 1 by lentivirus-driven shRNA expression). Finally, the lab initiated measurements of ion transport activities in ALI cultures that recently revealed novel pathways of maintaining airway surface liquid (ASL) volume. We have also successfully built a clinical trial environment around the themes of cystic fibrosis and chronic bronchitis/COPD for PI initiated and pharmaceutically sponsored trials. The cystic fibrosis trial environment at the University of Miami achieved therapeutic development center status by the Cystic Fibrosis Foundation’s Therapeutic Development Network in 2009.
- Schmid A., Meili D., Salathe M. Soluble adenylyl cyclase in health and disease. Biochim. Biophys. Acta – Molecular Basis of Disease. 2014: in press.
- Unwalla H., Ivonnet P., Dennis J.S., Conner G.E., Salathe M. TGF-ß1 and cigarette smoke inhibit the ability of ß2-agonists to enhance epithelial permeability. Am. J. Respir. Cell Mol. Biol 2014: in press.
- Gerovac B.J., Conner G.E., Baumlin N., Salathe M., Fregien N.L. Submersion and Hypoxia Inhibit Ciliated Cell Differentiation in a Notch Dependent Manner. Am. J. Respir. Cell Mol. Biol 2014: in press.
- Chen X., Baumlin N., Buck J., Levin L.R., Fregien N., Salathe M. A soluble adenylyl cyclase form targets to axonemes and rescues beat regulation in sAC knockout mice. Am. J. Respir. Cell Mol. Biol 2014: in press.
- Quittner A., Marciel K., Salathe M., O'Donnell A., Gotfried M., Ilowite J., Metersky M., Flume P., Lewis S., McKevitt M., Montgomery A.B., O'Riordan T., Barker A. A Preliminary Quality of Life Questionnaire-Bronchiectasis: A patient-reported outcome measure for bronchiectasis. Chest 2014, in press.
- Manzanares D., Srinivasan M., Salathe S.T., Ivonnet P., Baumlin N., Dennis J.S., Conner G.E., Salathe M. IFN-?-mediated reduction of large conductance, Ca2+ activated, voltage-dependent K+ (BK) channel activity in airway epithelial cells leads to mucociliary dysfunction. Am. J. Physiol. Lung Cell Mol. Physiol. 2014; 306: L453-62. PMCID: PMC3949055
- Conner G.E., Ivonnet P., Gelin M., Whitney P., Salathe M. H2O2 stimulates CFTR through an autocrine prostaglandin pathway using MRP4. Am. J. Respir. Cell Mol. Biol. 2013; 49:672-9. PMCID: PMC3824048