ArticleInternational journal of oral science2026
Spatially resolved single cell atlas deciphers SAA1 inflammatory epithelial cells.
Article in International journal of oral science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Disruption of epithelial integrity is a pivotal event in inflammation, disease pathogenesis, and tissue homeostasis. To investigate these processes in chronic inflammatory disease, we performed spatial transcriptomics integrated with single-cell RNA sequencing (scRNA-seq) on human gingival tissue, coupled with metagenomic analysis of matched subgingival plaque. This approach allowed in situ characterization of epithelial heterogeneity and microbiome-epithelium-connective tissue crosstalk. We identified a distinct inflammatory epithelial subpopulation (SAA1+Epi), situated within the junctional epithelium, that becomes activated through the TLR2-PITX2 axis by Porphyromonas gingivalis lipopolysaccharide. These SAA1+Epi cells secrete TGFβ, which induces an inflammatory program in the connective tissue by driving the differentiation of inflammation-associated fibroblasts (C3+FB) via the PI3K/Akt pathway. Concurrently, SAA1+Epi cells express chemotactic factors such as CXCL6 to recruit NK cells, thereby sustaining the inflammatory niche. The transcription factor PITX2 emerged as a critical regulator of SAA1+Epi differentiation; targeting PITX2 suppressed C3+FB induction and natural killer (NK) cells recruitment, ultimately attenuating periodontitis progression. Our findings position SAA1+Epi as a frontline responder to dysbiotic bacteria at the inflammatory interface and underscore its essential role in regulating epithelial-connective tissue homeostasis during inflammation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.