Airway epithelial differentiation and mucous cell metaplasia in chronic airway diseases
Mucous cell metaplasia and mucus over-production are hallmarks of almost all chronic airway diseases (e.g. asthma, chronic obstructive pulmonary diseases, cystic fibrosis, etc.) and significantly increase the morbidity and mortality. No therapy is available besides the mechanical suction. We are now investigating the function and regulation of mucin genes in asthma pathogenesis using both in vivo (gene targeting model, induced mouse model of asthma, as well as tissues and secretions from asthmatic patients) and in vitro (differentiated epithelial culture and cell line) models.
A new paradigm in virus-induced asthma exacerbation
Airway rhinovirus (RV) infection is the major cause of asthma exacerbation, a severe precipitation of the symptom in otherwise stable asthmatics who are often still under the routine medication. Thus, asthma exacerbation may have a different pathogenic mechanism that is largely unknown at present. Among different asthma-inducing allergens, Alternaria (Alt) is a fungal species that causes asthma in arid and semi-arid areas. In collaboration with the researchers at the Arizona Respiratory Center, we have found the shift of airway response to viral infection during Alt exposure, which promotes inflammation and depresses antiviral response. This shift causes a further increase of viral production and inflammation, similar to what would happen in the airways of asthma exacerbation. We are currently investigating the potential underlying mechanisms using both in vivo and in vitro models.
BS, Biochemistry, Nanjing University (China), 1996
PhD, Genetics, University of California Davis, 2001