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Lingzhi Wu1,2,3, Shiwen Wu1,2,3, Yuquan Deng1,2,3

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Indole-3-aldehyde (IAld) protects against periodontitis by strengthening the gingival epithelial barrier via the aryl hydrocarbon receptor (AhR) and Nrf2 pathways, reducing inflammation and bone loss.

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Area of Science:

  • Oral biology
  • Immunology
  • Microbiology

Background:

  • Periodontitis involves chronic inflammation and epithelial barrier dysfunction.
  • Indole-3-aldehyde (IAld), a tryptophan metabolite, is known to improve epithelial barriers via the aryl hydrocarbon receptor (AhR).

Purpose of the Study:

  • To investigate the role and mechanism of IAld in preserving the gingival epithelium in periodontitis through AhR activation.
  • To evaluate IAld's therapeutic potential for periodontitis.

Main Methods:

  • Established a mouse model of periodontitis, employing Micro-CT, histological, and 16S rRNA sequencing analyses.
  • Utilized in vitro assays (CCK-8, FITC-FD4 flux, Western blotting, immunofluorescence) on human gingival epithelial cells (hGECs) stimulated with P. gingivalis.
  • Performed RNA sequencing, immunofluorescence, and immunohistochemistry to explore molecular mechanisms.

Main Results:

  • IAld treatment in periodontitis mice reduced alveolar bone loss, periodontal inflammation, and activated the AhR pathway.
  • IAld increased tight junction protein expression (E-cadherin, Claudin1, Occludin, ZO-1) and modulated oral microbiota.
  • In vitro, IAld decreased hGEC permeability, upregulated CYP1A1, E-cadherin, and Claudin1, reduced ROS production, and enhanced Nrf2/HO-1 antioxidant pathways.

Conclusions:

  • IAld preserves gingival epithelial barrier integrity and function in periodontitis.
  • The protective mechanism involves AhR/Nrf2 signaling pathway activation and antioxidant responses.
  • IAld presents a promising therapeutic strategy for periodontitis treatment.