Summary
Introduction:
This summary will provide an overview of a scientific study investigating the impact of electronic cigarette (e-cig) vapor exposure on atherosclerosis development in apoE−/− mice, focusing on the role of Toll-like receptor 9 (TLR9) in this process. The study includes in vivo and in vitro experiments, as well as immunohistochemistry and flow cytometry analysis.
Key Points:
* apoE−/− mice exposed to e-cig vapor for 16 weeks showed increased atherosclerosis burden and intimal microscopic lesions compared to air-exposed mice.
* atherosclerotic plaques from e-cig-exposed mice had higher TLR9 expression compared to those from air-exposed mice.
* Similar results were observed in femoral arterial plaques from e-cig smokers compared to non-smokers.
* Pre-administration of TLR9 antagonist IRS869 significantly attenuated e-cig-exacerbated atherosclerosis development in apoE−/− mice.
* E-cig vapor exposure increased the frequency of CCR2+ classical monocytes and the expression of TLR9 in these cells.
* Plasma from e-cig-exposed mice induced TLR9 activation in hEK mTLR9 reporter cells, and cytoplasmic mtDNa from EVE-treated macrophages significantly induced the activation of TLR9.
* EVE treatment increased oxidative mtDNa lesion in cytoplasmic mtDNa, which is a stronger TLR9 stimulus than nonoxidized DNa.
Main Message:
The study suggests that e-cig vapor exposure exacerbates atherosclerosis development in apoE−/− mice, and this effect is mediated by TLR9 activation. The results provide evidence of the pro-atherosclerotic role of TLR9, and highlight the potential impact of e-cig vapor exposure on cardiovascular health. The study also highlights the potential of TLR9 inhibition as a therapeutic target for e-cig-associated atherosclerosis.
Citation
Li J, huynh L, Cornwell WD, et al. Electronic Cigarettes Induce Mitochondrial DNa Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated atherosclerosis. arteriosclerosis, thrombosis, and vascular biology. 2021;41(2):839-853. doi:10.1161/aTVBaha.120.315556
