1. Single-Cell Transcriptomic Atlas of Gingival Mucosa in Type 2 Diabetes.
- Author
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Wang, Q., Lin, W., Zhou, X., Lei, K., Xu, R., Zhang, X., Xiong, Q., Sheng, R., Song, W., Liu, W., and Yuan, Q.
- Subjects
TYPE 2 diabetes ,RNA sequencing ,GINGIVA ,PERIODONTITIS ,HYPERGLYCEMIA ,HOMEOSTASIS - Abstract
The oral gingival barrier is a constantly stimulated and dynamic environment where homeostasis is often disrupted, resulting in inflammatory periodontal diseases. Type 2 diabetes (T2D) has been reported to be associated with gingival barrier dysfunction, but the effect and underlying mechanism are inconclusive. Herein, we performed single-cell RNA sequencing (scRNA-seq) of gingiva from leptin receptor-deficient mice (db/db) to examine the gingival heterogeneity in the context of T2D. Periodontal health of control mice is characterized by populations of Krt14
+ -expressing epithelial cells and Col1a1+ -fibroblasts mediating immune homeostasis primarily through the enrichment of innate lymphoid cells. The db/db gingiva exhibited decreased epithelial/stromal ratio and dysfunctional barrier. We further observed stromal, particularly fibroblast immune hyperresponsiveness, linked to the recruitment of myeloid-derived cells at the db/db gingiva. Both scRNA-seq and histological analysis suggested the inflammatory signaling between fibroblasts and neutrophils as a potential driver of diabetes-induced periodontal damage. Notably, the "immune-like" stromal cells were wired toward the induction of gingival IL-17A hyperresponsiveness in db/db mice. Our work reveals that the "immune-like" fibroblasts with transcriptional diversity are involved in the innate immune homeostasis at the diabetic gingiva. It highlights a potentially significant role of these cell types in its pathogenesis. [ABSTRACT FROM AUTHOR]- Published
- 2022
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