# Association between Moraxella keratitis and advanced glycation end products

**Authors:** Hidenori Inoue, Koji Toriyama, Naoko Takahira, Shinobu Murakami, Hitoshi Miyamoto, Takashi Suzuki, Atsushi Shiraishi

PMC · DOI: 10.1038/s41598-024-58659-7 · Scientific Reports · 2024-04-05

## TL;DR

This study shows that advanced glycation end products in the cornea of diabetic patients increase the risk of Moraxella keratitis by promoting bacterial adhesion.

## Contribution

The study identifies a novel mechanism linking diabetes mellitus and Moraxella keratitis through AGEs-mediated bacterial adhesion.

## Key findings

- AGEs significantly increased Moraxella nonliquefaciens adhesion to corneal cells in vitro.
- Pyridoxamine, an AGE inhibitor, reduced bacterial adhesion in diabetic mouse corneas.
- Diabetic patients had a higher incidence of Moraxella keratitis compared to non-diabetic individuals.

## Abstract

Diabetes mellitus is recognized as a major predisposing factor for Moraxella keratitis. However, how diabetes mellitus contributes to Moraxella keratitis remains unclear. In this study, we examined Moraxella keratitis; based on the findings, we investigated the impact of advanced glycation end products (AGEs) deposition in the cornea of individuals with diabetic mellitus on the adhesion of Moraxella isolates to the cornea. A retrospective analysis of 27 culture-proven cases of Moraxella keratitis at Ehime University Hospital (March 2006 to February 2022) was performed. Moraxella isolates were identified using matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Among the patients, 30.4% had diabetes mellitus and 22.2% had the predominant ocular condition of using steroid eye drops. The species identified were Moraxella nonliquefaciens in 59.3% and Moraxella lacunata in 40.7% of patients. To investigate the underlying mechanisms, we assessed the effects of M. nonliquefaciens adherence to simian virus 40-immortalized human corneal epithelial cells (HCECs) with or without AGEs. The results demonstrated the number of M. nonliquefaciens adhering to HCECs was significantly increased by adding AGEs compared with that in controls (p < 0.01). Furthermore, in the corneas of streptozotocin-induced diabetic C57BL/6 mice treated with or without pyridoxamine, an AGE inhibitor, the number of M. nonliquefaciens adhering to the corneas of diabetic mice was significantly reduced by pyridoxamine treatment (p < 0.05). In conclusion, the development of Moraxella keratitis may be significantly influenced by the deposition of AGEs on the corneal epithelium of patients with diabetes mellitus.

## Linked entities

- **Chemicals:** pyridoxamine (PubChem CID 1052)
- **Diseases:** diabetes mellitus (MONDO:0005015)
- **Species:** Moraxella nonliquefaciens (taxon 478), Moraxella lacunata (taxon 477)

## Full-text entities

- **Genes:** RENBP (renin binding protein) [NCBI Gene 5973] {aka RBP, RNBP}
- **Diseases:** Diabetes mellitus (MESH:D003920), ocular condition (MESH:D020763)
- **Species:** Betapolyomavirus macacae (species) [taxon 1891767], Moraxella lacunata (species) [taxon 477], Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Moraxella nonliquefaciens (species) [taxon 478]
- **Cell lines:** C57BL/6 — Mus musculus (Mouse), Transformed cell line (CVCL_C0MU)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10997605/full.md

## References

58 references — full list in the complete paper: https://tomesphere.com/paper/PMC10997605/full.md

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Source: https://tomesphere.com/paper/PMC10997605