ArticleInflammation2026
Indole-3-aldehyde Preserves Gingival Epithelial Barrier Structure and Function Via AhR/Nrf2 Signaling Pathway.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Immunometabolic Remodeling in Osteosarcopenia: Inflammaging, Mitochondrial Dysfunction, Gut-Derived Metabolites and Therapeutic Opportunities.Metabolites · 2026Review
- Tryptophan Metabolism at the Crossroads of Immunity, Barrier Function, and the Microbiome in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Indole-3-aldehyde (IAld), an indole derivative of tryptophan metabolized by microorganisms, has been observed to improve epithelial barriers in multiple chronic inflammatory diseases through the aryl hydrocarbon receptor (AhR). This study aimed to elucidate the role and underlying mechanism of IAld in preserving the gingival epithelium via AhR activation in periodontitis. An experimental mouse model of periodontitis was established to assess the anti-periodontitis effect of IAld by using micro-computed tomography (Micro-CT), hematoxylin-eosin staining, immunohistochemical staining and 16S rRNA amplicon sequencing. Subsequently, CCK-8 assays, FITC-FD4 flux measurements, western blotting, and immunofluorescence staining were performed to confirm the protective effect of IAld on P. gingivalis-treated human gingival epithelial cells (hGECs) in vitro. Finally, RNA sequencing, immunofluorescence and immunohistochemical staining were used to thoroughly explore the underlying mechanism. We observed that in periodontitis mice, IAld treatment inhibited alveolar bone loss and periodontal tissue inflammation; activated the AhR pathway; increased the expression levels of E-cadherin, Claudin1, Occludin and ZO-1; and reshaped the oral microbial composition. In vitro, P. gingivalis-stimulated hGECs treated with IAld exhibited decreased FITC-FD4 permeability and upregulated expression of CYP1A1, E-cadherin and Claudin1 compared to the P. gingivalis group. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses revealed downregulation of oxidative stress pathways and overexpression of the antioxidants NrF2 and Hmox1. In vitro, IAld treatment reduced reactive oxygen species (ROS) production and upregulated the expression of Nrf2 and HO-1. Overall, our study demonstrated that IAld improved the function and integrity of the gingival epithelial barrier via the AhR/Nrf2 signaling pathway, thus providing a potential strategy for periodontitis treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.