Frontiers in pharmacology · 2026
A thermosensitive hydrogel encapsulating 2-DG alleviates periodontitis by inhibiting glycolysis and effector response of Th17 cells.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhao Ruowen, Li Jia, Yin Junhao, Xu Jiabao, Chen Changyu, Yan Jiayu, Chen Siyi, Fu Jiayao, Wu Junhua
Аннотация
OBJECTIVE: To investigate the mechanism of Th17 cells in immunomodulation during periodontitis and develop a localized drug delivery system based on glycolysis inhibition for safer and more effective therapeutic interventions.
METHODS: Periodontitis models were established via the use of IL17A-KO mice to evaluate the impact of Th17-related cytokine deficiency on pathological progression. Using single-cell RNA sequencing (scRNA-seq), we investigated the metabolic profile of CD4+ T cells under periodontitis conditions. The glycolysis inhibitor 2-deoxy-D-glucose (2-DG) was used to assess its ability to suppress CD4+ T-cell proliferation and Th17 differentiation. A thermosensitive PLGA-PEG-PLGA hydrogel encapsulating 2-DG was synthesized and locally administered to a murine periodontitis model.
RESULTS: IL17A-KO mice exhibited significantly attenuated alveolar bone resorption. Single-cell RNA sequencing revealed that, under periodontitis conditions, CD4+ T cells exhibited enhanced differentiation toward Th17 cells and increased glycolysis. The 2-DG hydrogel inhibited CD4+ T-cell expansion and Th17 polarization. Local application of the 2-DG hydrogel reduced periodontal inflammation, decreased bone destruction, and diminished granulocyte infiltration in gingival tissues.
CONCLUSION: Th17-cell differentiation exacerbates periodontitis progression, and glycolysis inhibition effectively modulates Th17-driven immunity. The localized 2-DG hydrogel delivery system presents a promising translational strategy for periodontitis management.
METHODS: Periodontitis models were established via the use of IL17A-KO mice to evaluate the impact of Th17-related cytokine deficiency on pathological progression. Using single-cell RNA sequencing (scRNA-seq), we investigated the metabolic profile of CD4+ T cells under periodontitis conditions. The glycolysis inhibitor 2-deoxy-D-glucose (2-DG) was used to assess its ability to suppress CD4+ T-cell proliferation and Th17 differentiation. A thermosensitive PLGA-PEG-PLGA hydrogel encapsulating 2-DG was synthesized and locally administered to a murine periodontitis model.
RESULTS: IL17A-KO mice exhibited significantly attenuated alveolar bone resorption. Single-cell RNA sequencing revealed that, under periodontitis conditions, CD4+ T cells exhibited enhanced differentiation toward Th17 cells and increased glycolysis. The 2-DG hydrogel inhibited CD4+ T-cell expansion and Th17 polarization. Local application of the 2-DG hydrogel reduced periodontal inflammation, decreased bone destruction, and diminished granulocyte infiltration in gingival tissues.
CONCLUSION: Th17-cell differentiation exacerbates periodontitis progression, and glycolysis inhibition effectively modulates Th17-driven immunity. The localized 2-DG hydrogel delivery system presents a promising translational strategy for periodontitis management.