Naphthoquinone enhances antigen-related airway inflammation in mice

¹ Environmental Health Sciences Division, National Institute for Environmental Studies, Ibaraki
² Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki
³ Dept of Health Science, Oita University of Nursing and Health Science, Oita
⁴ Dept of Environmental Medicine, Institute of Community Medicine, University of Tsukuba, Japan

^* To whom correspondence should be addressed. E-mail: htakano{at}nies.go.jp.

	Abstract

We have previously demonstrated that diesel exhaust particles (DEP) enhance antigen-related airway inflammation in mice (Takano et al., 1997). Further, our recent study has shown that organic chemicals in DEP, rather than their carbonaceous nuclei, are important contributors to the aggravating effects on the airway inflammation (Yanagisawa et al., 2006). However, the components in DEP responsible for the enhancing effects on the model remain to be identified. We investigated the effects of naphthoquinone (NQ), one of extractable chemical compounds of DEP, on antigen-related airway inflammation, local expression of cytokine proteins, and antigen-specific Igs production in mice. Pulmonary exposure to NQ dose-dependently aggravated antigen-related airway inflammation characterized 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 as compared with exposure to antigen or NQ alone. Also, NQ exhibited adjuvant activity for the antigen-specific production of IgG₁ and IgG_2a. These results provide the first experimental evidence that NQ can enhance antigen-related airway inflammation in vivo, and NQ can partly play a role in the pathogenesis of DEP toxicity on the condition.

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