Involvement of polycyclic aromatic hydrocarbons and endotoxin in macrophage expression of interleukin-33 induced by exposure to particulate matter

Nami Ishihara, Tomoaki Okuda, Hiroyuki Hagino, Ami Oguro, Yuto Tani, Hiroshi Okochi, Chiharu Tokoro, Yoshiaki Fujii-Kuriyama, Kouichi Itoh, Christoph F.A. Vogel, Yasuhiro Ishihara

研究成果: Article査読

1 被引用数 (Scopus)

抄録

Air pollutants are important factors that contribute to the development and/or exacerbation of allergic inflammation accompanied by asthma, but experimental evidence still needs to be collected. Interleukin 33 (IL-33) is closely involved in the onset and progression of asthma. In this study, we examined the effects of particulate matter (PM) on IL-33 expression in macrophages. PM2.5 collected in Yokohama, Japan by the cyclone device significantly induced IL-33 expression in human THP-1 macrophages, and the induction was clearly suppressed by pretreatment with the aryl hydrocarbon receptor (AhR) antagonist CH-223191 or the Toll-like receptor 4 (TLR4) antagonist TAK-242. PM2.5-induced IL-33 expression was significantly attenuated in AhR-knockout or TLR4-mutated macrophages, suggesting an important role of polycyclic aromatic hydrocarbons (PAHs) and endotoxin in IL-33 stimulation. PM samples derived from tunnel dust slightly but significantly induced IL-33 expression, while road dust PM did not affect IL-33 expression. The PAH concentration in tunnel dust was higher than that in road dust. Tunnel dust or road dust PM contained less endotoxin than PM2.5 collected in Yokohama. These data suggest that the potency of IL-33 induction could depend on the concentration of PAHs as well as endotoxin in PMs. Caution regarding PAHs and endotoxin levels in air pollutants should be taken to pre-vent IL-33-induced allergic inflammation.

本文言語English
ページ(範囲)201-210
ページ数10
ジャーナルJournal of Toxicological Sciences
47
5
DOI
出版ステータスPublished - 2022

ASJC Scopus subject areas

  • 毒物学

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