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.

Inhalation Toxicology
|March 9, 2019
PubMed
Abstract

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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