Journal of periodontal research · 2025
Toll-Like Receptor 7 Promotes Periodontal Inflammation and Alveolar Bone Resorption Through the NF-κB Signaling Pathway.
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Jing Rui, Lu Jiawei, Wang Ruiling, Xiong Zehui, Yang Yanan, Luo Lijun
Аннотация
AIM: To investigate the role of Toll-like receptor 7 (TLR7) in periodontitis and its potential mechanisms.
METHODS: TLR7 expression in periodontal tissues was analyzed using GEO database single-cell sequencing data and confirmed with gingival samples from healthy individuals and periodontitis patients. In vivo, a mouse model of periodontitis was used to assess the effect of M5049, the TLR7's inhibitor, on alveolar bone loss and inflammation. In vitro, mouse bone marrow-derived macrophages (BMDMs) were treated with Imiquimod to activate TLR7. The inflammatory response was further evaluated using Pg-LPS-stimulated BMDMs, with TLR7 knockdown and NF-κB inhibition by PDTC.
RESULTS: TLR7 expression in the gingival tissues of periodontitis patients was significantly elevated compared to healthy gingival tissues. In vivo, TLR7 inhibition reduced bone loss and inflammation, with decreased osteoclast formation and cytokine expression. In vitro, activation of TLR7 heightened inflammation; conversely, TLR7 knockdown and NF-κB inhibition diminished cytokine expression, suggesting a role for NF-κB in TLR7-mediated inflammatory responses.
CONCLUSION: TLR7 is upregulated in periodontitis and may promote the progression of the disease by activating the NF-κB signaling pathway, potentially serving as a therapeutic target. The findings reveal a novel role for TLR7 in periodontitis and highlight the TLR7-NF-κB axis as a key pathway in disease pathogenesis, with broader implications for understanding and treating inflammatory conditions.
METHODS: TLR7 expression in periodontal tissues was analyzed using GEO database single-cell sequencing data and confirmed with gingival samples from healthy individuals and periodontitis patients. In vivo, a mouse model of periodontitis was used to assess the effect of M5049, the TLR7's inhibitor, on alveolar bone loss and inflammation. In vitro, mouse bone marrow-derived macrophages (BMDMs) were treated with Imiquimod to activate TLR7. The inflammatory response was further evaluated using Pg-LPS-stimulated BMDMs, with TLR7 knockdown and NF-κB inhibition by PDTC.
RESULTS: TLR7 expression in the gingival tissues of periodontitis patients was significantly elevated compared to healthy gingival tissues. In vivo, TLR7 inhibition reduced bone loss and inflammation, with decreased osteoclast formation and cytokine expression. In vitro, activation of TLR7 heightened inflammation; conversely, TLR7 knockdown and NF-κB inhibition diminished cytokine expression, suggesting a role for NF-κB in TLR7-mediated inflammatory responses.
CONCLUSION: TLR7 is upregulated in periodontitis and may promote the progression of the disease by activating the NF-κB signaling pathway, potentially serving as a therapeutic target. The findings reveal a novel role for TLR7 in periodontitis and highlight the TLR7-NF-κB axis as a key pathway in disease pathogenesis, with broader implications for understanding and treating inflammatory conditions.