ArticleFrontiers in immunology2026
The miR-1260b-NFAT5 axis regulates inflammasome priming and M1 macrophage polarization in periodontitis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Macrophage-driven inflammatory programs and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome plays a critical role for periodontal tissue destruction; however, the transcriptional regulators that mediate these responses remain unclear. This study therefore examined the role of the microRNA-1260b (miR-1260b)-nuclear factor of activated T-cells 5 (NFAT5) axis in inflammatory macrophage responses relevant to periodontal disease. Methods: NFAT5 was identified as a candidate miR-1260b target using integrated bioinformatic screening and investigated through gain- and loss-of-function approaches in RAW264.7 macrophages. Inflammasome-related experiments were performed in J774A.1 macrophages using an LPS/ATP two-signal stimulation protocol. Further analyses included a ligature-induced mouse experimental periodontitis model with local NFAT5 small interfering RNA delivery, macrophage polarization assays in murine bone marrow-derived macrophages stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN-γ), and validation experiments in human peripheral blood mononuclear cell (PBMC)-derived macrophages. Results: Transfection with miR-1260b reduced NFAT5 expression and attenuated LPS-induced nuclear accumulation in macrophages. Discussion: These findings identify NFAT5 as a key regulator of inflammasome priming that contributes to inflammatory macrophage polarization in periodontal inflammation and suggest the miR-1260b-NFAT5 axis as a potential target for host-modulatory approaches.
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