IL-23 contributes to Particulate Matter induced allergic asthma in the early life of mice and promotes asthma susceptibility

This study aimed to investigate changes in allergic phenotypes and effects on allergen-specific memory T cells resulting from co-exposure of mice in the early life to PM and house dust mites (HDM) and to explore the role of interleukin-23 (IL-23) in this process. PM and low-dose HDM were administered intranasally in 4-day-old C57BL/6 mice. After confirming an increase in IL-23 expression in mouse lung tissues, changes in the asthma phenotype and lung effector/memory Th2 or Th17 cells were evaluated after intranasal administration of anti-IL-23 antibody (Ab) during co-exposure to PM and HDM. Evaluation was performed up to 7  weeks after the last administration. Co-exposure to PM and low-dose HDM resulted in increases in airway hyperresponsiveness (AHR), eosinophils, neutrophils, and persistent Th2/Th17 effector/memory cells, which were all inhibited by anti-IL-23 Ab administration. When low-dose HDM was administered t wice after a 7-week rest, mice exposed to PM and HDM during the previous early life period exhibited re-increases AHR, eosinophil count, HDM-specific IgG1, and effector/memory Th2 and Th17 cell populations. However, anti-IL-23 Ab administration during the early life period resulted in inhibition. Co -exposure to PM and low-dose HDM reinforced the allergic phenotypes and allergen-specific memory responses in early life of mice. During this process, IL-23 contributes to the enhancement of effector/memory Th2/Th17 cells and allergic phenotypes.Graphical AbstractExp...
Source: Journal of Molecular Medicine - Category: Molecular Biology Source Type: research