Dual-tissue single-cell analysis reveals a shared interferon-stimulated gene program and a predominantly non-neuronal trigeminal response in experimental periodontitis.

Authors

Xiaoqian Zhang, Xiaoqi Zhang

Published in

International immunopharmacology. Volume 191. Issue Pt 1. Pages 117586. Oct 22, 2026. Epub Oct 22, 2026.

Abstract

Periodontitis destroys the tooth-supporting tissues, yet whether a local periodontal lesion is accompanied by changes in the distal trigeminal sensory system at cell-type resolution is poorly defined. In ligature-induced periodontitis (male mice), we profiled the gingiva by single-cell and the trigeminal ganglion (TG) by single-nucleus RNA sequencing, integrating gene-set enrichment, regulon (SCENIC), communication (CellChat) and ligand-target (NicheNet) analyses with micro-computed tomography and histology, and tested the principal findings in individual mice by RT-qPCR (n = 8 per group) and immunofluorescence (n = 6 per group). Micro-CT and histology confirmed alveolar bone loss and osteoclast activity. Gingival cell-type composition shifted toward immune cells, whereas that of the TG changed only modestly. Descriptively, an interferon-stimulated gene (ISG) program with increased activity of ISGF3 regulons was enriched across nearly all cell types of both tissues. In individual mice, Isg15, Ifit3 and Oasl2 increased 4.7- to 9.3-fold in the gingiva and 3.4- to 3.9-fold in the TG. In the TG, ISG15-positive TUBULINβ3-negative non-neuronal cells rose from 8% to 67% of nucleated cells, whereas sensory neurons showed only a small ISG shift; a subset retained IFNAR expression. Ligand-target inference nominated gingival interferon ligands as candidate upstream regulators of the trigeminal ISG program. These data describe an interferon/ISG-associated program at the lesion and in the distal ganglion, consistent with type-I signaling in the gingiva; its interferon class in the ganglion, source, route and functional consequences remain to be established.

PMID:
42913199
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.

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