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Inhalation Toxicology
International Forum for Respiratory Research
Volume 30, 2018 - Issue 13-14
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Research Article

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

ORCID Icon, ORCID Icon, , , ORCID Icon, , , , , & show all
Pages 498-508 | Received 15 Aug 2018, Accepted 18 Dec 2018, Published online: 08 Mar 2019
 

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.

Acknowledgments

We thank Dr. Masayuki Kubo of US Environmental Protection Agency for his help with immunoblotting.

Disclosure statement

The authors have no conflict of interest associated with this manuscript.

Additional information

Funding

This work was supported in part by Japan Society for the Promotion of Science (JSPS) KAKENHI Grant Number JP16K15373 and JP18H03039.

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