critical role of interleukin-23 in development of asthma promoted by cigarette smoke

It has been recently reported that cigarette smoke exposure during allergen sensitization facilitates the development of allergic asthma; however, the underlying mechanisms remain elusive. we evaluated the role of interleukin (il-23) in a cigarette smoke extract (cse)-induced dermatophagoides pteronyssinus (dp)-allergic asthma mouse model. balb/c mice were exposed to cse during allergen sensitization period. anti-il-23p19 or il-23r antibody was administered during the sensitization period. and we evaluated several immunological responses. the expression of il-23 and il-23 receptor (il-23r) was examined in lung tissue. il-23 and il-23r expression was increased in the airway epithelium of dp/cse co-administered mice. cse administration during the sensitization promoted dp-allergic sensitization and the development of asthma phenotypes. additionally, the proportion of innate lymphoid type 2 cells (ilc2) was also increased by cse and dp co-instillation. anti-il-23 or il-23r antibody treatment during allergen sensitization significantly diminished phenotypes of allergic asthma and the ilc2 population. the levels of il-33 and thymic stromal lymphopoietin (tslp) were also significantly reduced by anti-il-23 or il-23r antibody treatment. il-23 thus play a significant role in cigarette smoke-induced allergic sensitization and asthma development. clinically, the increase in allergen sensitization due to cigarette exposure causes onset of asthma, and il-23 be important in this mechanism.