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Updated: Jan 28, 2026

Methods for Detecting Cough and Airway Inflammation in Mice
Published on: August 2, 2024
Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice
Keiki Ogino1, Kenjiro Nagaoka1, Tatsuo Ito1
1a Department of Public Health , Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science , Okayama , Japan.
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.
Insights
Particulate Matter 2.5 (PM2.5) proteins and trace elements contribute to allergic airway inflammation. Acid treatment reduced inflammation markers, suggesting these components are key drivers of PM2.5-induced allergic responses.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- Particulate Matter 2.5 (PM2.5) is a major air pollutant linked to respiratory diseases.
- The specific components of PM2.5 that drive allergic airway inflammation are not fully understood.
Purpose of the Study:
- To investigate the role of protein and trace element components of PM2.5 in allergic airway inflammation.
- To determine if altering these components affects the inflammatory response in a mouse model.
Main Methods:
- PM2.5 was treated with strong acid and high temperature to remove proteins and trace elements.
- BALB/c mice were exposed to saline, untreated PM2.5, or treated PM2.5.
- Allergic airway inflammation was assessed by measuring airway hyperresponsiveness, inflammatory cell counts, IgE levels, cytokine mRNA, and mucus production.
Main Results:
- Acid-treated PM2.5 significantly attenuated airway hyperresponsiveness, eosinophil infiltration, and specific cytokine mRNA levels (IL-13, CXCL3).
- Neutrophil infiltration and expression of certain inflammatory markers (MIP2α, EGFR, Nrf2, TLR4) increased after treatment.
- Treatment reduced PM2.5-bound proteins and acid-soluble trace elements (Zn, Cu, Pb, P, S, Mn, Fe, Ca, Ni), while increasing C, Si, and Cl.
Conclusions:
- PM2.5 induces allergic airway inflammation in mice.
- PM2.5-bound proteins and acid-soluble metals are implicated in the pathogenesis of PM2.5-induced allergic airway inflammation.
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