# Effect of Porphyromonas gingivalis lipopolysaccharide administration on non-alcoholic liver disease in Medaka fish

**Authors:** Ayano Ueki, Yukako Ito, Joe Sakamoto, Yasuhiro Kamei, Ayaka Yazawa, Shigeki Kamitani

PMC · DOI: 10.1093/femsmc/xtaf017 · FEMS Microbes · 2025-11-07

## TL;DR

This study shows that administering Porphyromonas gingivalis lipopolysaccharide to Medaka fish worsens non-alcoholic liver disease.

## Contribution

The novel finding is that Pg-LPS accelerates NASH progression in a Medaka model, linking periodontal disease to liver pathology.

## Key findings

- High-dose Pg-LPS increased liver weight and fat accumulation in Medaka.
- Pg-LPS caused liver fibrosis and altered intestinal microflora in the NASH model.
- Results suggest Pg-LPS exacerbates non-alcoholic liver disease in fish.

## Abstract

Recently, it has been reported that either infection of rodents with the periodontopathogenic Porphyromonas gingivalis (Pg) or administration of its lipopolysaccharide (Pg-LPS) to rodents with non-alcoholic steatohepatitis (NASH) causes progression and exacerbation of the disease. Thus, periodontal disease and NASH are closely related, and further research is required. Medaka (Oryzias latipes) has been used as an alternative model for studying human diseases in rodents. In this study, we investigated the association between NASH and Pg-LPS in a NASH model medaka, fed a high-fat diet for 12 weeks, and then injected intraperitoneally with Pg-LPS (low-dose Pg-LPS group: 1.5 mg/kg, high-dose Pg-LPS group: 15 mg/kg) once a week from 5 to 8 weeks. After 12 weeks, the effects of Pg-LPS administration on NASH pathology were evaluated. As a result, liver weight and liver weight/body weight values tended to be higher in the high-dose Pg-LPS group compared to the other groups. HE and Oil Red O staining of the liver showed increased fat accumulation with high-dose Pg-LPS. In addition, Sirius red staining of the liver found fibrosis only in the high-dose Pg-LPS group. These results suggest that Pg-LPS administration may accelerate the progression of the disease in the NASH model medaka.

Pg-LPS administration increased fat accumulation in the liver and changed intestinal microflora in the NAFLD/NASH model of Medaka.

## Linked entities

- **Diseases:** non-alcoholic steatohepatitis (MONDO:0007027), NAFLD (MONDO:0013209), NASH (MONDO:0007027)
- **Species:** Oryzias latipes (taxon 8090), Porphyromonas gingivalis (taxon 837)

## Full-text entities

- **Diseases:** non-alcoholic liver disease (MESH:D008108), periodontal disease (MESH:D010510), infection (MESH:D007239), NASH (MESH:D005235), fibrosis (MESH:D005355)
- **Chemicals:** Pg-LPS (-), Oil Red O (MESH:C011049), fat (MESH:D005223), lipopolysaccharide (MESH:D008070), HE (MESH:D006371)
- **Species:** Actinopterygii (fishes, superclass) [taxon 7898], Oryzias latipes (Japanese medaka, species) [taxon 8090], Porphyromonas gingivalis (species) [taxon 837], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12641535/full.md

## References

55 references — full list in the complete paper: https://tomesphere.com/paper/PMC12641535/full.md

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Source: https://tomesphere.com/paper/PMC12641535