Min-Jong Kang

My prior studies focused on the pathogenesis of cigarette-smoke (CS) -induced lung diseases such as chronic obstructive pulmonary disease (COPD), wherein we demonstrated that the IL-18 system plays an important role in the pathogenesis of CS-induced emphysematous lung destruction. These studies led me to question the effect of CS on innate immunity on the interaction between the host and microorganisms and, for this purpose, I had established a murine cigarette smoke and virus co-exposure model. These studies revealed important insight into the interaction between CS and the innate immunity resulting in a publication in the Journal of Clinical Investigation. In that study, we identified that CS smoke selectively augments respiratory antiviral innate immune responses via a MAVS-RLHs antiviral signaling pathway. To gain better understanding of the mechanisms, my laboratory is focusing on the role(s) of mitochondrial dysfunction and immune dysregulation in the setting of smoking exposure. By applying recent state-of-art knowledge of mitochondrial biology, our research goal is to establish mitochondrial dysfunction and mitochondrial injury/damage responses as a key event in the pathogenesis of COPD and CS-and virus-associated disorders and as such, to provide a new perspective of our understanding of COPD and CS-and virus-associated disorders.