Objective: To evaluate roles of IL-23 in short cigarette smoke exposure-induced HDM-allergic asthma mouse model
Methods: BALB/c mice were exposed to HDM and/or cigarette smoke extracts (CSE) during HDM sensitization period (day 1, 2, 3, and 14). Anti-IL-23p19 antibody was given during the sensitization period. And we analyzed several asthmatic phenotypes after last allergen challenge. In addition, we also analyzed the change of DC activation in LDLN and cytokines profile after last sensitization.
Results: CSE exposure during sensitization period promoted the development of HDM-allergic sensitization and asthma phenotypes. The proportion of innate lymphoid type 2 cells also increased by CSE and HDM co-exposure, compared to a single exposure. Anti-IL-23 antibody treatment during allergen sensitization period significantly diminished several phenotypes of allergic asthma. Anti-IL-23 treatment also reduced the recruitment of innate lymphoid type 2 cells. Along with, the activation of DC in LDLN was significantly reduced by anti-IL-23 after last sensitization.
Conclusion: IL-23 may play a significant role in the development of short cigarette smoke-induced allergic sensitization and asthma.