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

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)498-508
Number of pages11
JournalInhalation Toxicology
Volume30
Issue number13-14
DOIs
Publication statusPublished - 2018 Dec 6

Fingerprint

Metals
Inflammation
Bronchoalveolar Lavage Fluid
Trace Elements
Messenger RNA
Interleukin-13
Proteins
Acids
Chemokine CCL11
Fluids
Cyclonic Storms
Lung
Temperature
Interleukin-5
Mucus
Eosinophils
Interleukin-4
Immunoglobulin E
Neutrophils
Cytokines

Keywords

  • allergic airway inflammation
  • lung toxicity
  • MUC5ac
  • PM2.5
  • PM2.5-bound protein

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice. / Ogino, Keiki; Nagaoka, Kenjiro; Ito, Tatsuo; Takemoto, Kei; Okuda, Tomoaki; Nakayama, Shoji F.; Ogino, Noriyoshi; Seki, Yuka; Hamada, Hiroki; Takashiba, Shogo; Fujikura, Yoshihisa.

In: Inhalation Toxicology, Vol. 30, No. 13-14, 06.12.2018, p. 498-508.

Research output: Contribution to journalArticle

Ogino, K, Nagaoka, K, Ito, T, Takemoto, K, Okuda, T, Nakayama, SF, Ogino, N, Seki, Y, Hamada, H, Takashiba, S & Fujikura, Y 2018, 'Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice', Inhalation Toxicology, vol. 30, no. 13-14, pp. 498-508. https://doi.org/10.1080/08958378.2018.1561769
Ogino, Keiki ; Nagaoka, Kenjiro ; Ito, Tatsuo ; Takemoto, Kei ; Okuda, Tomoaki ; Nakayama, Shoji F. ; Ogino, Noriyoshi ; Seki, Yuka ; Hamada, Hiroki ; Takashiba, Shogo ; Fujikura, Yoshihisa. / Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice. In: Inhalation Toxicology. 2018 ; Vol. 30, No. 13-14. pp. 498-508.
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AU - Ito, Tatsuo

AU - Takemoto, Kei

AU - Okuda, Tomoaki

AU - Nakayama, Shoji F.

AU - Ogino, Noriyoshi

AU - Seki, Yuka

AU - Hamada, Hiroki

AU - Takashiba, Shogo

AU - Fujikura, Yoshihisa

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AB - 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.

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KW - lung toxicity

KW - MUC5ac

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KW - PM2.5-bound protein

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