Regulatory B cells induced by interleukin-35 inhibit inflammation and alveolar bone resorption in ligature-induced periodontitis

BackgroundRegulatory B cells (Bregs) have been reported to suppress immune responses and alveolar bone loss in murine periodontitis models. These cells could be induced by interleukin (IL)-35 which is increased upon periodontal inflammation. Thus, this study aimed to explore the role of Bregs induced by IL-35 in periodontitis. MethodsExperimental periodontitis was induced in mice by ligature. Two weeks after ligation, the test group was systemically treated with IL-35 for 1 week. Four weeks after ligation, all mice were euthanized, and alveolar bone loss was evaluated by microcomputed tomography. Cytokines associated with periodontitis were analyzed using reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Bregs in spleens, cervical lymph nodes, and periodontal tissues were detected by flow cytometry and immunofluorescence staining. ResultsIn the mouse model of periodontitis, IL-35 induced the expansion of CD1d(hi)CD5(+) B10 cells with increased interleukin-10 (IL-10) and IL-35 production. IL-35 administration also attenuated alveolar bone loss and reduced the levels of proinflammatory cytokines in situ. ConclusionsFollowing ligature-induced periodontitis in mice, IL-35 inhibited periodontal inflammation and alveolar bone resorption at least partially through the induction of B10 cells and IL-35(+) Bregs.

Automated summary

This study investigated the role of IL-35-induced Bregs in periodontitis. The results showed that IL-35 could expand CD1d(hi)CD5(+) B10 cells and increase the production of IL-10 and IL-35. Administration of IL-35 also reduced alveolar bone loss and inhibited inflammatory responses.