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Published on: April 3, 2017
Aqueous PM2.5 promotes lipid accumulation, classical macrophage polarisation and heat shock response
Lílian Corrêa Costa-Beber1, Rafael Kazmirczak Moraes1, Jéssica Marques Obelar Ramos1
1Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil.
Abstract:
Fine particulate matter (PM2.5) is an air pollutant that enhances susceptibility to cardiovascular diseases. Macrophages are the first immune cells to encounter the inhaled particles and orchestrate an inflammatory response. Given their role in atherosclerosis development, we investigated whether aqueous PM2.5 could elicit atherogenic effects by polarising macrophages to a pro-oxidative and pro-inflammatory phenotype and enhancing foam cell formation. The RAW264.7 macrophage cell line was exposed to PM2.5 for 48 h, with PBS as the control. Aqueous PM2.5 induced apoptosis and reduced cell proliferation. In surviving cells, we observed morphological, phagocytic, oxidative, and inflammatory features (i.e. enhanced iNOS, Integrin-1β, IL-6 expression), indicative of classical macrophage activation. We also detected an increase in total and surface HSP70 levels, suggesting macrophage activation. Further, exposure of high-cholesterol diet-fed mice to PM2.5 resulted in aortic wall enlargement, indicating vascular lesions. Macrophages exposed to PM2.5 and non-modified low-density lipoprotein (LDL) showed exacerbated lipid accumulation. Given the non-oxidised LDL used and the evidence linking inflammation to disrupted cholesterol negative feedback, we hypothesise that PM2.5-induced inflammation in macrophages enhances their susceptibility to transforming into foam cells. Finally, our results indicate that exposure to aqueous PM2.5 promotes classical macrophage activation, marked by increased HSP70 expression and that it potentially contributes to atherosclerosis.
Insights
Fine particulate matter (PM2.5) exposure activates macrophages, promoting inflammation and potentially contributing to atherosclerosis. This study reveals PM2.5
Area of Science:
- Environmental Health
- Immunology
- Cardiovascular Research
Background:
- Fine particulate matter (PM2.5) is a significant air pollutant linked to cardiovascular diseases.
- Macrophages play a critical role in initiating inflammatory responses upon encountering inhaled particles, influencing atherosclerosis development.
Purpose of the Study:
- To investigate the atherogenic effects of aqueous PM2.5 on macrophages.
- To determine if PM2.5 exposure polarizes macrophages towards a pro-oxidative and pro-inflammatory phenotype.
- To assess the impact of PM2.5 on macrophage foam cell formation.
Main Methods:
- Exposure of RAW264.7 macrophage cell line to aqueous PM2.5 for 48 hours.
- Assessment of macrophage apoptosis, proliferation, morphology, phagocytosis, oxidative stress, and inflammatory marker expression (iNOS, Integrin-1β, IL-6).
- Evaluation of heat shock protein 70 (HSP70) levels as an indicator of macrophage activation.
- In vivo study involving high-cholesterol diet-fed mice exposed to PM2.5 to assess vascular effects.
- Co-exposure of macrophages with PM2.5 and low-density lipoprotein (LDL) to examine lipid accumulation.
Main Results:
- Aqueous PM2.5 induced apoptosis and reduced proliferation in macrophages.
- Surviving macrophages exhibited features of classical activation, including enhanced iNOS, Integrin-1β, IL-6, and HSP70 expression.
- PM2.5 exposure in mice led to aortic wall enlargement, indicative of vascular lesions.
- Macrophages exposed to both PM2.5 and LDL showed increased lipid accumulation.
- PM2.5 exposure promoted classical macrophage activation and potentially contributes to atherosclerosis.
Conclusions:
- Exposure to aqueous PM2.5 promotes classical macrophage activation, evidenced by increased HSP70 expression.
- PM2.5-induced inflammation in macrophages may enhance their susceptibility to foam cell formation.
- These findings suggest a potential mechanism by which PM2.5 contributes to the development of atherosclerosis.
