Sangwoon Chung, PhD

Inhibiting airway inflammation by inhaled corticosteroids is a mainstay of asthma therapy. One type of asthma is called neutrophilic asthma, which is characterized by increased levels of neutrophils (a type of white blood cell) in the airways. The most relevant clinical trait of neutrophilic severe asthma is its poor response to standard asthma treatments, thus additional effective treatments are urgently needed for these patients. It is important to identify critical factors that contribute to increased numbers of neutrophils in asthmatic patients whose symptoms are poorly controlled by conventional therapy. To meet this challenge, we will study a novel therapeutic tool using optimized exosomes—cellular components that exist outside the cell—to provide pre-clinical evidence for mitigating the inflammatory asthmatic features for neutrophilic severe asthma patients. Update: Recent work from our laboratory has identified FoxO1 transcription factor, a known modulator of immune functions, as a key regulator of immune cells called macrophages in mouse models of asthma. We found inhibiting FoxO1 significantly mitigated the functional changes associated with asthma. We expect that blocking FoxO1 will reduce a protein called IRF4, which the lead to the reduction of allergic inflammation in the airways. This will provide preclinical data to support a future study seeking a novel therapeutic benefit for difficult-to-control (refractory) asthma.

Update: We employed a mouse model of severe asthma that mimics the complex immune response that has been identified in patients with severe asthma. We have made progress in understanding of how allergic inflammation is exacerbated. Our findings are leading us closer to a novel treatment for neutrophilic severe late-onset asthma.