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Airborne fine particulate matter causes murine bronchial hyperreactivity via MAPK pathway-mediated M3 muscarinic

Rong Wang1,2, Xue Xiao1, Zhenxing Shen3

  • 1Department of Pharmacology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Environmental Toxicology
|February 27, 2016
PubMed

Insights

Airborne fine particulate matter 2.5 (PM2.5) exposure increases bronchial hyperreactivity by upregulating muscarinic receptors. This effect is mediated by p38 and MEK1/2 mitogen-activated protein kinase (MAPK) pathways, highlighting a key molecular mechanism of respiratory distress.

Area of Science:

  • Environmental Toxicology
  • Respiratory Physiology
  • Molecular Mechanisms of Disease

Background:

  • Airborne fine particulate matter 2.5 (PM2.5) is a significant environmental risk factor for human health.
  • The precise molecular pathways through which PM2.5 induces respiratory dysfunction remain largely unelucidated.

Purpose of the Study:

  • To investigate the hypothesis that PM2.5 causes bronchial hyperreactivity by upregulating muscarinic receptors via the mitogen-activated protein kinase (MAPK) pathway.
  • To elucidate the role of specific MAPK pathways in PM2.5-induced airway responses.

Main Methods:

  • Isolated rat bronchi segments were cultured with varying concentrations of PM2.5.
  • Contractile responses were measured using myography.
  • M3 muscarinic receptor mRNA and protein expression were quantified using qRT-PCR and immunohistochemistry, respectively.
  • Specific MAPK pathway inhibitors (p38, MEK1/2, JNK) were employed to assess their effects.

Main Results:

  • PM2.5 exposure (1.0 µg/mL for 24 h) significantly enhanced muscarinic receptor-mediated bronchial contraction.
  • PM2.5 exposure led to increased mRNA and protein expression of M3 muscarinic receptors.
  • Inhibition of p38 and MEK1/2 MAPK pathways attenuated PM2.5-induced hyperreactivity and receptor upregulation.
  • JNK pathway inhibition did not affect PM2.5-induced effects.

Conclusions:

  • Airborne PM2.5 upregulates muscarinic receptors, leading to bronchial hyperreactivity and enhanced contractility.
  • The p38 and MEK1/2 MAPK pathways are implicated in the molecular mechanism of PM2.5-induced airway dysfunction.
Keywords:
MAPK pathwayairborne fine particulate matterbronchial hyperreactivitymuscarinic receptor

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