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Indoor PM2.5 from coal combustion aggravates ovalbumin-induced asthma-like airway inflammation in BALB/c mice

Jie Yu1, Kebin Li1, Jie Xu1

  • 1School of Public Health, Zunyi Medical University, Zunyi, People's Republic of China.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|April 11, 2019
PubMed

Insights

Indoor coal combustion particulate matter (PM2.5) exposure worsens airway inflammation in asthmatic mice. This study shows PM2.5 exacerbates allergic airway disease by increasing inflammatory responses and altering immune cell balance.

Area of Science:

  • Environmental Health
  • Immunology
  • Pulmonary Medicine

Background:

  • Indoor air pollution from coal combustion is a significant global health concern.
  • Particulate matter (PM2.5) is a major component of indoor air pollution linked to respiratory diseases.
  • Asthma is a chronic inflammatory airway disease affecting millions worldwide.

Purpose of the Study:

  • To investigate the effects of indoor PM2.5 exposure from coal combustion on airway inflammation in a mouse model of asthma.
  • To determine the impact of PM2.5 exposure on immune responses, cytokine production, and lung pathology in asthmatic mice.

Main Methods:

  • Ovalbumin (OVA)-induced asthma model in BALB/c mice.
  • Exposure to PM2.5 from indoor coal combustion (mean concentration 156.95 μg/m3) and OVA.
  • Assessment of inflammatory markers (IL-4, IFN-γ, GM-CSF, IL-8, TGF-β1) in serum and bronchoalveolar lavage fluid (BALF).
  • Analysis of gene expression (IL-4, IFN-γ, Foxp3 mRNA) in lung tissue.
  • Histopathological examination of lung tissue for inflammatory cell infiltration and airway remodeling.

Main Results:

  • PM2.5 exposure combined with OVA significantly increased IL-4 and decreased IFN-γ production.
  • Elevated levels of granulocyte-macrophage colony-stimulating factor and IL-8, with decreased transforming growth factor-β1, were observed in BALF.
  • Increased IL-4 mRNA and decreased IFN-γ and Foxp3 mRNA expression in lung tissue of PM2.5+OVA exposed mice.
  • PM2.5+OVA exposure led to neutrophil sequestration, goblet cell proliferation, and significant inflammatory cell infiltration in the airways.

Conclusions:

  • Indoor PM2.5 from coal combustion exacerbates airway inflammation and allergic immune responses in asthmatic mice.
  • PM2.5 exposure alters the balance of pro-inflammatory and anti-inflammatory cytokines, contributing to airway pathology.
  • These findings highlight the detrimental role of indoor coal combustion-derived PM2.5 in worsening asthma severity and airway structural changes.
Keywords:
PMairway inflammationasthmacoal combustionindoorlung tissue

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