Gary Hunninghake, M.D. (Full Member)
Director, Institute for Clinical and Translational, University of Iowa
Professor, Dept. of Internal Medicine, University of Iowa
Faculty, Medical Scientist Training Program, University of Iowa
Sterba Professor, University of Iowa
Director, Graduate Program in Translational Biomedical Research, University of Iowa

http://www.int-med.uiowa.edu/Divisions/Pulmonary/Directory/GaryHunninghake.html

Research Interest    

Dr. Hunninghake's research interests pertain to the molecular mechanisms of gene regulation in macrophage epithelial cells and animal models of pulmonary fibrosis and granuloma formation. These studies evaluate the roles of specific transcription factors and their regulation by various second messenger pathways. A second area of interest, which is highly relevant to virus-directed gene therapies to the lung, includes evaluating the regulation of cytokine gene expression by viruses. These studies determine how viruses, including influenza and RSV, manipulate cellular expression of host genes. Animal models are used to understand the genetic control of molecular mechanisms underlying the pulmonary fibrosis and granuloma formation that take place in the lung following viral infection. Additionally, the laboratory has used recombinant adenoviruses in mouse models to identify systemic cytokine responses that alter survival in the presence of LPS and bacterial loads. These studies are particularly relevant to understanding vector mucosal immune responses in the CF lung and how they may be altered by bacterial infection. Dr. Hunninghake's expertise in viral responses in the lung has made him a valuable resource within the center's Vector Development and Mucosal Immune Response research program. In addition, Dr. Hunninghake is a highly respected researcher in lung biology and has previously served as President of the American Thoracic Society.

Selected Publications

Hansdottir, S., Monick M.M., Hinde, S.L, Lovan, N., Look, D.C. and Hunninghake, G.W. Respiratory Epithelial Cells Convert Inactive Vitamin D to its Active Form: Potential Effects on Host Defense. J Immunol. 181:7090-7099, 2008. PMID: 18981129

Monick, M.M., Powers, L.S., Barrett, C., Hinde, S., Ashare, A., Groskreutz, D., Nyunoya, T., Coleman, M., Spitz, D.R. and Hunninghake, G.W. Constitutive ERK MAP activity regulates macrophage ATP production and mitochondrial integrity. J Immunol. 180:7485-7496, 2008.

Groskreutz, D.J., Monick, M.M., Yarovinsky, T.O., Powers, L.S., Quelle, D.E., Varga, S.M., Look, D.C., and Hunninghake, G.W. Respiratory syncytial virus decreases p53 protein to prolong survival of airway epithelial cells. J Immunol. 179(5): 2741-2747, 2007.

Monick, M.M., Powers, L.S., Hassan, I., Groskreutz, D., Yarovinsky, T.O., Barrett, C.W., Castilow, E.M., Tifrea, D., Varga, S.M., and Hunninghake, G.W. Respiratory syncytial virus synergizes with Th2 cytokines to induce optimal levels of TARC/CCL17. J Immunol. 179(3):1648-58, 2007.

Publications from Gene Therapy Center

Publications from PubMed