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PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar

Miao He1,2, Takamichi Ichinose2, Seiichi Yoshida2

  • 1Department of Environmental Health, School of Public Health, China Medical University, Shenyang, 110122, China.

Journal of Applied Toxicology : JAT
|May 31, 2017
PubMed

Insights

Particulate matter 2.5 (PM2.5) causes lung inflammation through oxidative stress in alveolar cells, not solely via the LPS/MyD88 pathway in macrophages. N-acetylcysteine (NAC) effectively reduced inflammation, particularly when combined with polymyxin B (PMB).

Area of Science:

  • Environmental Health
  • Toxicology
  • Pulmonary Medicine

Background:

  • Particulate matter 2.5 (PM2.5) is a significant air pollutant linked to chronic obstructive pulmonary disease.
  • The precise mechanisms of PM2.5-induced lung inflammation, involving inflammation and oxidative stress, require further elucidation.

Purpose of the Study:

  • To investigate the in vitro and in vivo mechanisms of PM2.5-induced lung inflammation.
  • To identify key biomarkers and pathways involved in PM2.5 exposure.
  • To evaluate the therapeutic potential of N-acetylcysteine (NAC) and polymyxin B (PMB) in mitigating PM2.5-induced lung injury.

Main Methods:

  • In vitro studies using RAW264.7 cells and mouse bone marrow-derived macrophages (BMDMs) from wild-type and MyD88 knockout mice.
  • In vitro studies using MLE-12 cells (mouse alveolar cell line).
  • In vivo study involving intratracheal instillation of PM2.5 in BALB/c mice, followed by analysis of bronchoalveolar lavage fluid.

Main Results:

  • PM2.5 induced inflammatory responses in macrophages via the LPS/MyD88 pathway, which were attenuated by PMB.
  • PM2.5 induced oxidative stress and inflammation in MLE-12 cells, with N-acetylcysteine (NAC) showing significant attenuation.
  • In vivo, PM2.5 caused severe lung inflammation, which was effectively reduced by NAC, especially in combination with PMB.

Conclusions:

  • PM2.5 induces lung inflammation through both LPS/MyD88-dependent pathways in macrophages and oxidative stress in alveolar cells.
  • Oxidative stress in type II alveolar cells appears to be the predominant mechanism driving PM2.5-induced lung inflammation.
  • NAC demonstrates therapeutic potential in mitigating PM2.5-induced lung inflammation, suggesting a role in managing air pollution-related respiratory diseases.
Keywords:
MLE-12 cellsMyD88 KOPM2.5lung inflammationmacrophagesoxidative stress

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