The current authors have previously demonstrated that
diesel exhaust particles (
DEP) enhance
antigen-related airway
inflammation in mice. Furthermore, a recent study has shown that
organic chemicals in
DEP, rather than their carbonaceous nuclei, are important contributors to the aggravating effects of airway
inflammation. However, the components in
DEP responsible for the enhancing effects on the model remain to be identified. The current authors investigated the effects of
naphthoquinone (NQ), one of the extractable chemical compounds of
DEP, on
antigen-related airway
inflammation, local expression of
cytokine proteins, and
antigen-specific
immunoglobulin (Ig) production in mice. Pulmonary exposure to NQ dose-dependently aggravated
antigen-related airway
inflammation, as characterised by infiltration of eosinophils and lymphocytes around the airways and an increase in goblet cells in the bronchial epithelium. Combined exposure to NQ and
antigen enhanced the local expression of
interleukin (IL)-4,
IL-5, eotaxin, macrophage
chemoattractant protein-1 and keratinocyte
chemoattractant, compared with exposure to
antigen or NQ alone. Also, NQ exhibited adjuvant activity for the
antigen-specific production of
IgG(1) and
IgG(2a). These results provide the first experimental evidence that
naphthoquinone can enhance
antigen-related airway
inflammation in vivo, and that
naphthoquinone can, to some extent, partly play a role in the pathogenesis of
diesel exhaust particle toxicity on the condition.