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Published on: September 26, 2018
PM2.5-induced inflammation and lipidome alteration associated with the development of atherosclerosis based on a
Jingyi Zhang1, Shuang Liang1, Ruihong Ning1
1Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China.
Abstract:
Epidemiological studies have confirmed that PM2.5 could contribute to the development of atherosclerosis accompanied with lipids dysregulation. However, the lipids biomarkers involved in this progress remain largely unknown. In this study, a targeted lipidomic approach was used to find out the possible lipid biomarkers involved in the development of atherosclerosis after PM2.5 exposure or during a recovery period. Also, we assessed the pro-atherosclerosis effects of PM2.5 and follow-up influence using pulse wave (PW) Doppler ultrasound, oil red O staining and H&E staining. The vascular stiffness was elevated after 2-month PM2.5 exposure and might persist after 1-month recovery. While the lesions mostly concentrated in the aortic arch was significantly increased in 2-month PM2.5 exposure group and remained an increasing trend after 1-month recovery. The expressions of pro-inflammatory cytokines detected by Mouse Inflammation Array were elevated after ApoE-/- mice treated with PM2.5 for 2-month and restored following 1-month recovery. Yet, IL-10 was significantly decreased during 1-month recovery. Additionally, the targeted lipidomic analysis demonstrated that cholesterol ester (CE), phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (SM) were significantly increased while lysophosphatidylethanolamine (LPE), lysophosphatidylcholine (LPC), diacylglycerol (DG), triacylglycerol (TG) were reduced after 2-month PM2.5 exposure, indicating that PM2.5 could disrupt glycerophospholipids, glycerolipids and sphingolipids metabolism. And a persistent impact of PM2.5 on glycerophospholipids and glycerolipids metabolism was found after 1-month recovery. Our study demonstrated that PM2.5-induced inflammation response might promote atherosclerotic lesions probably through lipid dysregulation, and the influence probably persisted after 1-month recovery.
Insights
Fine particulate matter (PM2.5) exposure promotes atherosclerosis by disrupting lipid metabolism and increasing inflammation. These effects, including elevated vascular stiffness and aortic arch lesions, may persist even after a recovery period.
Area of Science:
- Environmental Health
- Cardiovascular Research
- Metabolomics
Background:
- Epidemiological studies link PM2.5 exposure to atherosclerosis and lipid dysregulation.
- Specific lipid biomarkers involved in PM2.5-induced atherosclerosis remain largely unidentified.
Purpose of the Study:
- To identify lipid biomarkers associated with atherosclerosis development following PM2.5 exposure.
- To evaluate the pro-atherosclerotic effects of PM2.5 and its persistent impact during recovery.
Main Methods:
- Targeted lipidomics to analyze lipid profiles.
- Pulse wave Doppler ultrasound, oil red O, and H&E staining to assess vascular changes and lesions.
- Mouse Inflammation Array to measure pro-inflammatory cytokines.
Main Results:
- PM2.5 exposure increased vascular stiffness, aortic arch lesions, and pro-inflammatory cytokines.
- Significant alterations in lipid metabolism were observed, including increased cholesterol esters and phospholipids, and decreased lysophospholipids and triglycerides.
- These changes, particularly in glycerophospholipid and glycerolipid metabolism, showed a persistent impact post-recovery.
Conclusions:
- PM2.5-induced inflammation and lipid dysregulation promote atherosclerotic lesion development.
- The detrimental effects of PM2.5 on lipid metabolism and atherosclerosis may persist after a recovery period.
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