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Fine particulate matter (PM2.5) enhances airway hyperresponsiveness (AHR) by inducing necroptosis in BALB/c mice

Yunxia Zhao1, Huiran Zhang2, Xiuna Yang3

  • 1Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China; Department of Respiratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050051, China.

Environmental Toxicology and Pharmacology
|April 16, 2019
PubMed
Abstract

Insights

Prolonged exposure to fine particulate matter (PM2.5) significantly increased airway hyperresponsiveness (AHR) in mice. These PM2.5-induced lung damages are mediated by necroptosis-related inflammation.

Area of Science:

  • Environmental Health
  • Toxicology
  • Pulmonary Medicine

Background:

  • Fine particulate matter (PM2.5) exposure is a global health concern.
  • Understanding the mechanisms of PM2.5-induced lung injury is crucial.

Purpose of the Study:

  • To investigate the effects of prolonged PM2.5 exposure on mouse trachea and lungs.
  • To determine if PM2.5-induced lung damage is caused by necroptosis.

Main Methods:

  • Mice were exposed to PM2.5 or filtered air for 8 weeks.
  • Airway hyperresponsiveness (AHR), inflammation, and necroptosis markers (TUNEL, Fas, RIPK3, MLKL) were assessed.

Main Results:

  • PM2.5 exposure significantly increased AHR, neutrophils, bronchitis, and inflammation.
  • Necroptosis markers (TUNEL, Fas, RIPK3, MLKL) were elevated in the PM2.5 group.

Conclusions:

  • PM2.5 exposure enhances AHR in mice.
  • Necroptosis-related inflammation plays a key role in PM2.5-induced lung injury.
Keywords:
Airway HyperresponsivenessFine Particulate MatterNecroptosis

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