IL-23 plays a significant role in the augmentation of particulate matter-mediated allergic airway inflammation

It has been recently that particulate matter (PM) exposure increases the risk and exacerbation of allergic asthma. However, the underlying mechanisms and factors associated with increased allergic responses remain elusive. We evaluated IL-23 and IL-23R (receptor) expression, as well as changes in the asthmatic phenotype in mice administered PM and a low dose of house dust mite (HDM). Next, changes in the phenotype and immune responses were evaluated after intranasal administration of anti-IL-23 antibody during co-exposure to PM and low-dose HDM. We also performed in vitro experiments to investigate the effect of IL-23. IL-23 expression was significantly increased in Epcam+CD45- and CD11c+ cells, while that of IL-23R was increased in Epcam+CD45- cells only in mice administered PM and low-dose HDM. Administration of anti-IL-23 antibody led to decreased airway hyperresponsiveness, eosinophils, and activation of dendritic cells, reduced populations of Th2 Th17, ILC2, the level of IL-33 and granulocyte-macrophage colony-stimulating factor (GM-CSF). Inhibition of IL-23 in PM and low-dose HDM stimulated airway epithelial cell line resulted in decreased IL-33, GM-CSF and affected ILC2 and the activation of BMDCs. PM augmented the phenotypes and immunologic responses of asthma even at low doses of HDM. Interestingly, IL-23 affected immunological changes in airway epithelial cells.

Automated summary

Recent research has shown that exposure to particulate matter (PM) increases the risk and exacerbation of allergic asthma, but the underlying mechanisms and factors associated with increased allergic responses are still unclear. This study investigated the expression of IL-23 and IL-23R, as well as changes in the asthmatic phenotype, in mice exposed to PM and a low dose of house dust mite (HDM). The results showed that IL-23 expression was significantly increased in certain cell types, and administration of anti-IL-23 antibody led to decreased airway hyperresponsiveness and immune activation. In addition, IL-23 affected immunological changes in airway epithelial cells. These findings suggest that IL-23 may play a role in the development and exacerbation of asthma caused by PM exposure and low-dose HDM.