Aqueous PM 2.5 promotes lipid accumulation, classical macrophage polarisation and heat shock response.

Autor: Corrêa Costa-Beber L; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil. Electronic address: liliantutty@hotmail.com., Kazmirczak Moraes R; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil., Marques Obelar Ramos J; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil., Meira Martins LA; Department of Physiology, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil., Toquetto AL; Universidade Regional do Noroeste do Estado do Rio Grande do Sul (UNIJUÍ), Research Group in Physiology, Postgraduate Program in Integral Health Care, Ijuí, Rio Grande do Sul State, Brazil., Fursel Pacheco J; Universidade Regional do Noroeste do Estado do Rio Grande do Sul (UNIJUÍ), Research Group in Physiology, Postgraduate Program in Integral Health Care, Ijuí, Rio Grande do Sul State, Brazil., Resende Farias H; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil., Gioda A; Department of Chemistry, Pontifícia Universidade Católica do Rio de Janeiro (PUC-Rio), Departamento de Química, Rio de Janeiro, RJ, Brazil., Antunes de Oliveira V; Universidade Regional do Noroeste do Estado do Rio Grande do Sul (UNIJUÍ), Research Group in Physiology, Postgraduate Program in Integral Health Care, Ijuí, Rio Grande do Sul State, Brazil., de Oliveira J; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil., Costa Rodrigues Guma FT; Department of Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS), Ramiro Barcelos, 2600, 90035-003, Annex, Porto Alegre, Rio Grande do Sul, Brazil.
Jazyk: angličtina
Zdroj: Chemosphere [Chemosphere] 2024 Sep; Vol. 363, pp. 142987. Date of Electronic Publication: 2024 Jul 31.
DOI: 10.1016/j.chemosphere.2024.142987
Abstrakt: Fine particulate matter (PM 2.5 ) 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 PM 2.5 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 PM 2.5 for 48 h, with PBS as the control. Aqueous PM 2.5 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 PM 2.5 resulted in aortic wall enlargement, indicating vascular lesions. Macrophages exposed to PM 2.5 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 PM 2.5 -induced inflammation in macrophages enhances their susceptibility to transforming into foam cells. Finally, our results indicate that exposure to aqueous PM 2.5 promotes classical macrophage activation, marked by increased HSP70 expression and that it potentially contributes to atherosclerosis.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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