Background and objective
Previous studies have demonstrated that our recombinant bacille Calmette‐Guerin (rBCG), which expresses Der p2 in house dust mite (Der p2 rBCG) suppresses asthmatic airway inflammation by regulating the phenotype and function of dendritic cells (DC) and reprogramming T helper (Th) 0 cell differentiation into different T cell (Th1/Th2/Treg) subtypes. However, the exact role of Der p2 rBCG in reprogramming Th17 differentiation and the relevant mechanisms are not known. The aim of this study was to examine whether Der p2 rBCG‐mediated inhibition of allergic airway inflammation is mediated by regulating Th17 differentiation in a murine asthma model.
Methods
Primary mouse bone marrow‐derived dendritic cells (BMDC) were infected with Der p2 rBCG and adoptively transferred to Der p2‐intranasally sensitized mice. The role of Der p2 rBCG‐BMDC on the regulation of airway inflammation and Th17 cell differentiation was assessed.
Results
Adoptive transfer of Der p2 rBCG‐BMDC suppressed airway inflammation and mucin secretion. Der p2 rBCG‐BMDC inhibited excessive Th17 immune responses but not BCG‐BMDC. Furthermore, Der p2 rBCG decreased jagged‐2 and increased delta‐like‐4 expressions on BMDC to a greater extent than BCG.
Conclusions
These findings suggest that DC plays a key role in Der p2 rBCG‐induced immunoregulation. Der p2 rBCG also displayed a potent inhibitory effect on Th17 differentiation, and these findings increase our understanding of the cellular basis of Der p2 BCG‐mediated inhibition of asthma.