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Proteomic Analysis of Human Macrophage Polarization Under a Low Oxygen Environment
Published on: January 7, 2019
Direct effects of airborne PM2.5 exposure on macrophage polarizations
Qingjie Zhao1, Hui Chen2, Tao Yang2
1Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing, China; State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Background:
Exposure of atmospheric particulate matter with an aerodynamic diameter less than 2.5μm (PM2.5) is epidemiologically associated with illnesses. Potential effects of air pollutants on innate immunity have raised concerns. As the first defense line, macrophages are able to induce inflammatory response. However, whether PM2.5 exposure affects macrophage polarizations remains unclear.
Methods:
We used freshly isolated macrophages as a model system to demonstrate effects of PM2.5 on macrophage polarizations. The expressions of cytokines and key molecular markers were detected by real-time PCR, and flow cytometry. The specific inhibitors and gene deletion technologies were used to address the molecular mechanisms.
Results:
PM2.5 increased the expression of pro-inflammatory cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor alpha (TNFα). PM2.5 also enhanced the lipopolysaccharide (LPS)-induced M1 polarization even though there was no evidence in the change of cell viability. However, PM2.5 significantly decreased the number of mitochondria in a dose dependent manner. Pre-treatment with NAC, a scavenger of reactive oxygen species (ROS), prevented the increase of ROS and rescued the PM2.5-impacted M1 but not M2 response. However, mTOR deletion partially rescued the effects of PM2.5 to reduce M2 polarization.
Conclusions:
PM2.5 exposure significantly enhanced inflammatory M1 polarization through ROS pathway, whereas PM2.5 exposure inhibited anti-inflammatory M2 polarization through mTOR-dependent pathway.
General Significance:
The present studies suggested that short-term exposure of PM2.5 acts on the balance of inflammatory M1 and anti-inflammatory M2 macrophage polarizations, which may be involved in air pollution-induced immune disorders and diseases. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
Insights
Exposure to fine particulate matter (PM2.5) significantly alters macrophage polarization, increasing inflammatory M1 responses via reactive oxygen species (ROS) and decreasing anti-inflammatory M2 responses through the mTOR pathway. This impacts immune balance and may contribute to air pollution-related diseases.
Area of Science:
- Environmental Health
- Immunology
- Cell Biology
Background:
- Atmospheric particulate matter (PM2.5) exposure is linked to various illnesses.
- Air pollutants can affect innate immunity, with macrophages playing a key role in inflammatory responses.
- The impact of PM2.5 on macrophage polarization remains largely unclear.
Purpose of the Study:
- To investigate the effects of PM2.5 exposure on macrophage polarization.
- To elucidate the molecular mechanisms underlying PM2.5-induced changes in macrophage phenotypes.
- To understand how PM2.5 influences the balance between pro-inflammatory and anti-inflammatory macrophage responses.
Main Methods:
- Freshly isolated macrophages were used as a model system.
- Gene and protein expression of cytokines and key molecular markers were analyzed using real-time PCR and flow cytometry.
- Specific inhibitors and gene deletion techniques were employed to investigate molecular pathways, including reactive oxygen species (ROS) and mTOR.
Main Results:
- PM2.5 exposure increased the expression of pro-inflammatory cytokines (GM-CSF, IL-6, IL-1β, TNFα).
- PM2.5 enhanced lipopolysaccharide (LPS)-induced M1 polarization and decreased mitochondrial numbers in a dose-dependent manner.
- NAC pre-treatment (ROS scavenger) rescued M1 polarization, while mTOR deletion partially rescued M2 polarization.
Conclusions:
- PM2.5 exposure promotes M1 polarization via the ROS pathway.
- PM2.5 inhibits M2 polarization through an mTOR-dependent pathway.
- Short-term PM2.5 exposure disrupts the balance of macrophage polarization, potentially contributing to immune disorders.
