Porphyromonas gingivalis triggers lipid metabolism disorders in atherosclerosis through the PPARγ-LXRα‑ABCA1/ABCG1 signaling pathway

The present study aimed to analyze the effects of Porphyromonas gingivalis infection on atherosclerosis caused by lipid metabolism disorders in apolipoprotein E‑knockout (ApoE^‑/‑) mice. A total of 20 male ApoE^‑/‑ mice were randomly divided into two groups (n=10/group). The mice in the ApoE^‑/‑ infected group were orally inoculated with P. gingivalis for 6 weeks, whereas those in the ApoE^‑/‑ control group were orally administered PBS. Blood biochemistry was performed to determine the serum levels of total cholesterol (TC), triglyceride (TG), high‑density lipoprotein (HDL) and low‑density lipoprotein (LDL) in the mice. ELISA was used to determine the protein levels of monocyte chemotactic protein‑1 (MCP‑1), IL‑6 and oxidized LDL (ox‑LDL) in the serum of mice. In addition, a comprehensive comparison of atherosclerotic plaques and pathological changes in the liver between the P. gingivalis‑infected group and the control group was performed. Subsequently, reverse transcription‑quantitative PCR was performed to measure the expression levels of genes related to the peroxisome proliferator‑activated receptor γ (PPARγ)‑liver X receptor α (LXRα)‑ATP‑binding cassette transporter (ABC)A1/ABCG1 pathway in the liver. A total of 6 weeks after P. gingivalis inoculation, the levels of TC, TG, LDL, ox‑LDL, IL‑6 and MCP‑1 in the serum of the ApoE^‑/‑ P. gingivalis‑infected group were significantly higher compared with those in the ApoE‑/‑ control group, whereas HDL levels were significantly lower. Furthermore, compared with in the ApoE^‑/‑ control group and the C57B6/L with P. gingivalis infection group, the severity of atherosclerotic plaques in the ApoE^‑/‑ group infected with P. gingivalis was more severe, and the vacuolar degeneration of liver cells was more pronounced, manifested by decreased levels of ABCA1, ABCG1, LXRα and PPARγ. In conclusion, P. gingivalis may amplify lipid metabolism disorders and aggravate the symptoms of atherosclerosis through the CD36‑mediated PPARγ‑LXRα‑ABCA1/ABCG1 signaling pathway.