Areas of Research
Immune regulation of airway inflammation
Our group was one of the few that raised the significance of innate immune regulation of asthmatic airway inflammation. We demonstrated the regulatory role of airway epithelium-derived lectin-like molecules CD23 and lung collectins (SP-A and SP-D) in the onset and resolution of airway inflammation. We also showed that group 2 innate lymphoid cells (ILC2) were critical in mediating inflammatory cell influx into the airways and eliciting airway hyperresponsiveness.
Psychosocial stress and asthma
Role of glucocorticoid insensitivity – Glucocorticoid responsiveness plays an important role in asthma. We described that increased allergic airway inflammation and impaired lung function can be induced by chronic psychosocial stress. We also demonstrated that this effect was associated with an impaired function of the glucocorticoid receptor. We have shown that glucocorticoid dependent immune regulatory genes (such as surfactant protein D) are dysregulated in the airway epithelium due to stress. We aim to establish a novel asthma sub-phenotype according to the stress status and steroid responsiveness of patients.
Surfactant protein D (SP-D) in regulation of airway inflammation
We were the first to describe the negative feedback this lung collectin exerts on proinflammatory dendritic cell function and Th2-type cytokines in asthma. We are currently investigating how SP-D affects the function of dendritic cells, macrophages and NK and innate lymphoid cells in the lung under homeostatic and inflammatory conditions, including influenza A virus infection, allergen or ozone exposure, and psychosocial stress.
Airway epithelium biology
Our lab is particularly interested in how epithelial and dendritic cells cooperate in the initiation and resolution of the inflammatory airway response to environmental exposures (allergen, ozone, cigarette smoke, psychosocial stress and viral infections). Our recent data suggest that mucosal immune responses play an essential role in maintenance of pulmonary tissue homeostasis.