Particulate matter could accelerate the development of atherosclerosis in mice. - GreenMedInfo Summary
Acceleratory effects of ambient fine particulate matter on the development and progression of atherosclerosis in apolipoprotein E knockout mice by down-regulating CD4CD25Foxp3regulatory T cells.
Toxicol Lett. 2019 Nov ;316:27-34. Epub 2019 Sep 9. PMID: 31513887
OBJECTIVE: Atherosclerosis is an autoimmune inflammatory disease that is closely associated with long-term exposure to fine particulate matter (PM2.5). CD4CD25Foxp3regulatory T cells (Tregs) play a critical role in the regulation of T cell-mediated immune responses, and the depletion of CD4CD25Foxp3Tregs has been thought to play a prominent role in atherosclerosis. Therefore, we investigated the association between the CD4CD25Foxp3Tregs population and atherosclerotic development in ApoEmice exposed to PM2.5.
METHODS: We employed a real-world system to subject 40 ApoEmice to ambient inhalation of PM2.5 (PM2.5 group, n = 20) or filtered air (FA group, n = 20) for 12 weeks. PM2.5 source apportionment, atherosclerotic lesions within aorta, lipid deposition and plaque accumulation in whole artery, serum level of inflammatory factors and lipid profiles, CD4CD25Foxp3Tregs population in splenocytes, Foxp3 protein and mRNA expressions in descending aorta and spleen were quantified, respectively.
RESULTS: The daily average concentration of PM2.5 was 57.4 ± 25.6 μg/m. Atherosclerotic lesions within aorta, lipid deposition and plaque accumulation in whole artery, serum levels of IL-6, TNF-α, TC and LDL-C in the PM2.5 group increased significantly compared to the FA group. Whereas, serum levels of IL-10 and TGF-β, CD4CD25Foxp3Tregs population in splenocytes, Foxp3 protein and mRNA expressions in descending aorta and spleen in the PM2.5 group decreased significantly compared to the FA group.
CONCLUSION: These results suggest that PM2.5 could accelerate the development of atherosclerosis in ApoEmice, which is related to CD4CD25Foxp3Tregs down-regulation, as well as lipid deposition and systemic inflammation.