Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice

Keiki Ogino, Kenjiro Nagaoka, Tatsuo Ito, Kei Takemoto, Tomoaki Okuda, Shoji F. Nakayama, Noriyoshi Ogino, Yuka Seki, Hiroki Hamada, Shogo Takashiba, Yoshihisa Fujikura

研究成果: Article査読

5 被引用数 (Scopus)

抄録

Background: The aim of this study was to investigate the protein and trace element components of PM2.5 and their contribution to the allergic airway inflammation in BALB/c mice. Methods: PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice. Allergic airway inflammation was compared between the three groups (saline, pure PM2.5 and treated PM2.5) by evaluating airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF) cells, serum IgE, the mRNA of various cytokine (IL-4, IL-5, IL-13, eotaxin-1 and CXCL3), mucus protein mRNA (MUC5ac and MUC5b) and the filtration of inflammatory cells in the lung. Results: The treatment of PM2.5 with a strong acid at a high temperature attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation. On the contrary, the percentage of neutrophils in BALF, mRNA expression of MIP2α, EGFR, Nrf2, and TLR4 and 4-OH-2-nonenal levels in the lung was increased. Moreover, the treatment of the PM2.5 reduced PM2.5-bound proteins as well as the percentages of the trace elements in PM2.5 in the order Zn > Cu > Pb > P > S > Mn > Fe > Ca > Ni, whereas the percentage of C, Si and Cl increased. Conclusions: PM2.5 collected by of the cyclone system induced allergic airway inflammation in mice. PM2.5-bound proteins and acid-soluble metals may be involved in the pathogenesis of PM2.5-induced allergic airway inflammation.

本文言語English
ページ(範囲)498-508
ページ数11
ジャーナルInhalation Toxicology
30
13-14
DOI
出版ステータスPublished - 2018 12 6

ASJC Scopus subject areas

  • 毒物学
  • 健康、毒物学および変異誘発

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