Research Summary
Dr. Mitzner’s research is focused on the structural basis of physiologic lung function and how this normal structure manifests itself in pathologic situations and environmental exposures. Current work is concerned with understanding the mechanisms that underlie the chronic lung tissue destruction that occurs in emphysema. These functional and immunological studies in the mouse are directed toward investigating mechanisms of alveolar destruction with age or with emphysematous lesions. How this tissue destruction impacts the interaction between the lung parenchyma and airways plays a key role in the ability to breathe in this pathology, and ongoing work is involved in studying this interaction. Additional funded work involves evaluating methods of impairing the ability of airway smooth muscle to shorten as a possible treatment of asthma, called bronchial thermoplasty.
Lab
Dr. Mitzner's lab is housed in the Department of Environmental Health Sciences at the Johns Hopkins Bloomberg School of Public Health. His research team studies basic mechanisms behind the physiologic and pathologic manifestations of lung diseases such as emphysema and asthma. Current research investigates why chronic changes continue to exist in the lungs long after the initial insults are completely gone. Such insults lead to tissue damage, causing immunologic responses that seem to persist almost indefinitely. This manifestation is analyzed using state-of-the-art phenotyping in whole animal models simultaneously with assessment of the immunologic status of cells and interactive signaling.
Lab Website: Mitzner Laboratory
Selected Publications
An SS, Mitzner W, Tang WY, Ahn K, Yoon AR, Huang J, Kilic O, Yong HM, Fahey JW, Kumar S, Biswal S, Holgate ST, Panettieri RA, Solway J, Liggett SB. “An inflammation-independent contraction mechanophenotype of airway smooth muscle in asthma.” Journal of Allergy and Clinical Immunology. 2016. In press.
Lin AHY, Shang Y, Mitzner W, Sham JSK, Tang WY. “Aberrant DNA methylation of phosphodiesterase 4D alters airway smooth muscle cell phenotypes.” American Journal of Respiratory Cell and Molecular Biology. 2016 Feb;54(2):241-249.
Seccombe LM, Peters MJ, Brown RH, Mitner W. “Lung density in extremely large healthy lungs.” Chest. 2016 Jan;149(1):291-292.
Lagesse HAD, Anidi IU, Craig JM, Limjunyawong N, Poupore AK, Mitnzer W, Scott AL. “Recruited monocytes modulate malaria-induced lung injury through CD36-mediated clearance of sequestered infected erythrocytes.” Journal of Leukocyte Biology. 2016 May;99(5):659-71.
Wagner EM, Jenkins J, Schmieder A, Eldridge L, Zhang Q, Moldobaeva A, Zhang H, Allen JS, Yang X, Mitzner W, Keupp J, Caruthers SD, Wickline SA, Lanza GM. “Angiogenesis and airway reactivity in asthmatic Brown Norway rats.” Angiogenesis. 2015:18(1).