Modulation of lectin-like oxidized low-density lipoprotein receptor-1 by Porphyromonas gingivalis promoting progression of atherosclerosis in apolipoprotein E-/- mice

• Published in: Journal of dental sciences Vol. 20; no. 2; pp. 754 - 763
• Main Authors: Zhang, Shengnan, Liu, Jianru, Ouyang, Xiangying, Lyu, Peiying, Wang, Yuanbo, Zhong, Jinsheng
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.04.2025; Association for Dental Sciences of the Republic of China; Elsevier
• Subjects: Advanced Basic Science; Atherosclerosis; Dentistry; LOX-1; Macrophage; Original; Plaque; Poly(I:C); Porphyromonas gingivalis; Porphyromonas gingivalis; Poly(I:C); LOX-1; Atherosclerosis; Plaque; Macrophage
• ISSN: 1991-7902; 2213-8862
• DOI: 10.1016/j.jds.2024.10.015

Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice. Using apolipoprotein E (APOE)-/- mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined. Results showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6. These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis.