Spatiotemporally Responsive BEC Nanoplatform Targets Neutrophils to Reprogram Immune Crosstalk and Alleviate Periodontal Inflamm-aging in Periodontitis (PRJCA050578)
Current antibacterial biomaterial-based strategies for chronic periodontitis fail to address the regenerative impairment caused by periodontal inflamm-aging, a systemic pro-inflammatory state driven by macrophage pyroptosis and subsequent gingival fibroblast dysfunctionNeutrophils, as early initiators, release neutrophil extracellular traps that critically trigger macrophage pyroptosis, yet their roles in immune recruitment and antimicrobial defense necessitate precise rather than broad inhibition. Studies have shown that interfering with the crosstalk between neutrophils and macrophages can effectively reverse periodontal aging. Functional analyses revealed that BEC NPs suppressed neutrophil extracellular trap formation via dual mechanisms: scavenging reactive oxygen species to preserve mitochondrial integrity and stabilizing the actin cytoskeleton to inhibit nuclear translocation of neutrophil elastase and myeloperoxidase. Furthermore, BEC NPs mitigated NET-induced macrophage pyroptosis and reversed the senescent phenotype of gingival fibroblasts.