We have recently demonstrated that
naphthoquinone (NQ), one of extractable chemical compounds of
diesel exhaust particles (
DEP), enhances
antigen-related airway
inflammation with goblet cell
hyperplasia in mice (Inoue et al. in Eur Respir J 209(2):259-267, 2007). Further, NQ has enhanced lung expressions of
interleukin (IL)-4 and
IL-5. However, the effects of NQ on other cardinal features of
asthma have not been completely investigated. The aim of the present study was to evaluate the effects of NQ on airway responsiveness on the model. Vehicle, NQ,
ovalbumin (OVA), or NQ + OVA was administered intratarcheally to ICR mice for 6 weeks. Twenty-four hours after the last instillation, lung histology, lung functions such as total respiratory system resistance (R) and Newtonian resistance (R (n)), and
protein level of
IL-13 and
mRNA level for MUC5AC in the lung were examined. Repetitive exposure to NQ aggravated
antigen-related
lung inflammation. NQ alone enhanced R and R (n) as compared to vehicle without statistical significance. OVA alone or NQ plus OVA showed increases in R and R (n), which was prominent in NQ plus OVA (P < 0.05 vs. vehicle). Combined exposure to NQ and OVA elevated the levels of
IL-13 and MUC5AC in the lung as compared with exposure to NQ or OVA alone. These results indicate that NQ can enhance
airway hyperresponsiveness in the presence or absence of an
antigen. Also, amplified lung expressions of
IL-13 and MUC5AC might partly contribute to the deterioration of
asthma features by NQ.