Suil Kim
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Assistant Professor
Background
Dr. Kim received his A.B. and M.S. degrees from the University of Chicago. He received his M.D. and Ph.D. degrees from the University of Michigan and completed residency training in Internal Medicine at the University of Pittsburgh. Moving west, he completed a clinical fellowship in Pulmonary and Critical Care Medicine at the University of California San Francisco, followed by a research fellowship with Dr. Jay Nadel in the Cardiovascular Research Institute. He was on the pulmonary faculty at UCSF before joining Oregon Health & Science University in 2011. His major academic activities include basic research and clinical medicine as an attending physician at the Portland VA Medical Center. Dr. Kim’s research focuses on the airway epithelium, the body’s primary responders to inhaled invaders (eg, bacteria, cigarette smoke). He investigates basic mechanisms that exaggerate airway epithelial responses in chronic inflammatory airway diseases such as chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and lung cancer. In COPD and CF, exaggerated production of mucins and neutrophil chemokines results in airway mucous plugging and in neutrophilic inflammation, leading to progressive airway obstruction and ultimately to death. In lung adenocarcinoma, increased proliferative responses and escape from immune surveillance lead to a pro-tumor phenotype. Epidermal growth factor receptor (EGFR) activation has been shown to induce airway epithelial production of mucins and neutrophil chemokines and to induce pro-tumor responses in lung adenocarcinoma cells, but the mechanisms that exaggerate these responses in disease states remain unknown. The goal of Dr. Kim’s research is to identify these mechanisms. Recently, he discovered that G-protein-coupled receptor activation can lead to repeated EGFR activation over time, exaggerating pro-inflammatory airway epithelial responses. Through this work, he hopes to discover novel targets for the effective treatment of exaggerated airway epithelial responses in diseases such as COPD, CF and lung cancer. SELECTED PUBLICATIONS 1. Kim S, Shim JJ, Burgel P-R, Ueki I, Dao-Pick T, Tam D, and Nadel JA (2002). IL-13-induced CCSP expression in airway epithelium: role of EGF-R signaling pathway. Am J Physiol Lung Cell Mol Physiol 283: L67-75. 2. Kim S, and Nadel JA (2004). Role of neutrophils in mucus hypersecretion in COPD and implications for therapy. Treat Respir Med 3: 147-159. 3. Kim S, Schein AJ, and Nadel JA (2005). E-cadherin promotes EGFR-mediated cell differentiation and MUC5AC mucin expression in cultured human airway epithelial cells. Am J Physiol Lung Cell Mol Physiol 289: L1049-1060. 4. Kim S, Shao MX-G, and Nadel JA (2005). Mucus production, secretion, and clearance. In: Mason RJ, Broaddus VC, Murray JF, Nadel JA, editors. Textbook of Respiratory Medicine, 4th ed., Philadelphia, Saunders, pp 330-354. 5. Koff JL, Shao M, Kim S, Ueki IF, and Nadel JA (2006). Pseudomonas LPS accelerates wound repair via activation of a novel epithelial cell signaling cascade. J Immunol 177: 8693-8700. 6. Kim S, and Nadel JA (2009). Fibrinogen binding to ICAM-1 promotes EGFR-dependent mucin production in human airway epithelial cells. Am J Physiol Lung Cell Mol Physiol 297: L174-183. 7. Kim S, Lewis C, and Nadel JA (2011). CCL20/CCR6 feedback exaggerates epidermal growth factor receptor-dependent MUC5AC mucin production in human airway epithelial (NCI-H292) cells. J Immunol 186: 3392-3400. 8. Kim S, Lewis C, and Nadel JA (2011). Epidermal growth factor receptor reactivation induced by E-Prostanoid-3 receptor- and tumor necrosis factor-alpha-converting enzyme-dependent feedback exaggerates interleukin-8 production in airway cancer (NCI-H292) cells. Exp Cell Res 317: 2650-2660.
Summary of Current Research
Dr. Kim sees patients at the Portland VA Medical Center. He has a joint appointment at OHSU.
