Lactic acid bacteria prevent both periodontitis and atherosclerosis exacerbated by periodontitis in spontaneously hyperlipidemic mice

Ryoki Kobayashi, Tomomi Hashizume-Takizawa, Tomoko Kurita-Ochiai

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

Background and Objective: Recent studies have shown a link between periodontal disease and cardiovascular disease. We have previously reported that oral administration of Porphyromonas gingivalis (Pg) accelerates atherosclerosis in apolipoprotein E-deficient spontaneously hyperlipidemic (Apoeshl) mice. This study evaluated the potential of lactic acid bacteria (LAB) to change the intestinal flora changes induced by periodontopathic bacteria and to prevent/slow down the development of atherosclerosis. Methods: Lactobacillus gasseri O3-2 (Lg) was orally intubated in Apoeshl mice for 5 weeks. Three weeks after oral intubation, the mice were orally infected with Pg for 2 weeks. Results: Thirty days after the last infection with Pg, Lg+Pg-treated mice showed a significant reduction in alveolar bone loss compared to the Pg-treated group. The Lg treatment restored the Pg-induced intestinal flora disturbance to normal. Furthermore, a significant decrease in atherosclerotic plaque lesion size and suppressed inflammatory cytokine production in the aorta were detected in the Lg + Pg-treated group. In contrast, blood concentrations of TMAO, histidine, and carnitine were enhanced by the Lg treatment but decreased by Lg + Pg treatment. Conclusion: These results suggest that oral Lg treatment is effective in preventing periodontitis and atherosclerosis.

Original languageEnglish
Pages (from-to)753-760
Number of pages8
JournalJournal of Periodontal Research
Volume56
Issue number4
DOIs
Publication statusPublished - Aug 2021

Keywords

  • atherosclerosis
  • lactic acid bacteria
  • periodontitis
  • Porphyromonas gingivalis

Fingerprint

Dive into the research topics of 'Lactic acid bacteria prevent both periodontitis and atherosclerosis exacerbated by periodontitis in spontaneously hyperlipidemic mice'. Together they form a unique fingerprint.

Cite this