Particulate matter exposure induces the autophagy of macrophages via oxidative stress-mediated PI3K/AKT/mTOR pathway

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Ruijun Su1, Xiaoting Jin2, Weifang Zhang3

  • 1Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Wucheng Rood 92, Taiyuan 030006, China.

Chemosphere
|October 18, 2016
PubMed

Insights

Fine particulate matter (PM2.5) exposure harms immune cells by inducing macrophage autophagy. This process is driven by oxidative stress and the PI3K/AKT/mTOR pathway, explaining PM2.5

Area of Science:

  • Environmental toxicology
  • Immunology
  • Cellular and molecular toxicology

Background:

  • Epidemiological studies link fine particulate matter (PM2.5) to immunotoxicity.
  • The precise molecular mechanisms underlying PM2.5-induced immunotoxicity remain incompletely understood.
  • Investigating cellular responses, particularly autophagy in macrophages, is crucial for elucidating these mechanisms.

Purpose of the Study:

  • To investigate the effects of PM2.5 exposure on macrophage autophagy.
  • To elucidate the molecular pathways involved in PM2.5-induced immunotoxicity.
  • To explore the role of oxidative stress and the PI3K/AKT/mTOR pathway in PM2.5-mediated cellular effects.

Main Methods:

  • Exposure of Sprague-Dawley (SD) rats and Raw264.7 macrophage cells to varying concentrations of PM2.5 via intratracheal instillation for 2 months.
  • Assessment of immune cell counts in pulmonary macrophages.
  • Analysis of autophagy markers (LC3, p62) at mRNA and protein levels.
  • Evaluation of oxidative stress and the involvement of N-acetylcysteine (NAC) as a reactive oxygen species (ROS) inhibitor.
  • Investigation of the PI3K/AKT/mTOR signaling pathway.

Main Results:

  • PM2.5 exposure led to a decrease in immune cell numbers within SD rat pulmonary macrophages.
  • PM2.5 exposure induced macrophage autophagy in a dose-dependent manner, evidenced by increased LC3 and decreased p62 levels.
  • PM2.5 exposure triggered significant oxidative stress.
  • Supplementation with NAC reversed the adverse effects of PM2.5, including reduced autophagy and oxidative stress.
  • The PI3K/AKT/mTOR pathway was activated by PM2.5 exposure, and NAC exhibited inhibitory effects on this pathway.

Conclusions:

  • PM2.5 exposure induces autophagy in pulmonary macrophages through oxidative stress-mediated activation of the PI3K/AKT/mTOR pathway.
  • This autophagy induction is a key molecular mechanism contributing to PM2.5-induced immunotoxicity.
  • Findings provide a theoretical basis for understanding the environmental toxicology of PM2.5 and its impact on immune function.
Keywords:
AutophagyOxidative stressPI3K/AKT/mTOR pathwayPM(2.5)Pulmonary macrophage

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