Journal of oral microbiology · 2025
Bifidobacterium longum inhibits Aggregatibacter actinomycetemcomitans- associated gingival epithelial ferroptosis and protects cellular junctions.
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Sun Xiaojiao, Wang Zehui, Qiu Dan, Yan Di, Cao Kun, Jun-Ichi Sasaki, Satoshi Imazato, Qin Xu, Sun Xiaojuan
Аннотация
BACKGROUND: Periodontal pathogens disrupt the gingival epithelial barrier, but the molecular links among junctional damage, ferroptosis, and inflammation remain unclear.
OBJECTIVE: To investigate whether Bifidobacterium longum (BL) counteracts Aggregatibacter actinomycetemcomitans (Aa)-induced junctional injury via regulation of ferroptosis in human gingival epithelial cells (HGECs).
DESIGN: Oral microbiota differences between periodontitis patients and healthy controls were analyzed using 16S rRNA sequencing, combined with GSE16134 bioinformatics analysis. HGECs were exposed to Aa (1 × 10⁴ CFU/ml) and treated with BL (1 × 10⁸ CFU/ml) or ferrostatin-1 (Fer-1, 2 μM). Cell viability, mitochondrial morphology, ROS, junction proteins (CDH1, CLDN1), ferroptosis markers (SLC7A11, GPX4, NFE2L2), and inflammatory cytokines (IL-6, IL-10, TNF) were assessed.
RESULTS: Bioinformatics revealed enrichment of junction-related pathways associated with ferroptosis. Aa induced mitochondrial damage, ROS accumulation, suppression of ferroptosis-protective signaling and junction proteins, and pro-inflammatory cytokine imbalance. BL significantly restored mitochondrial integrity, ferroptosis-related signaling, epithelial junctions, and inflammatory homeostasis, with effects comparable to or exceeding Fer-1.
CONCLUSION: Aa disrupts gingival epithelial integrity through ferroptosis-mediated oxidative and inflammatory damage. BL effectively suppresses this cascade and protects epithelial junctions, highlighting its therapeutic potential for periodontitis.
OBJECTIVE: To investigate whether Bifidobacterium longum (BL) counteracts Aggregatibacter actinomycetemcomitans (Aa)-induced junctional injury via regulation of ferroptosis in human gingival epithelial cells (HGECs).
DESIGN: Oral microbiota differences between periodontitis patients and healthy controls were analyzed using 16S rRNA sequencing, combined with GSE16134 bioinformatics analysis. HGECs were exposed to Aa (1 × 10⁴ CFU/ml) and treated with BL (1 × 10⁸ CFU/ml) or ferrostatin-1 (Fer-1, 2 μM). Cell viability, mitochondrial morphology, ROS, junction proteins (CDH1, CLDN1), ferroptosis markers (SLC7A11, GPX4, NFE2L2), and inflammatory cytokines (IL-6, IL-10, TNF) were assessed.
RESULTS: Bioinformatics revealed enrichment of junction-related pathways associated with ferroptosis. Aa induced mitochondrial damage, ROS accumulation, suppression of ferroptosis-protective signaling and junction proteins, and pro-inflammatory cytokine imbalance. BL significantly restored mitochondrial integrity, ferroptosis-related signaling, epithelial junctions, and inflammatory homeostasis, with effects comparable to or exceeding Fer-1.
CONCLUSION: Aa disrupts gingival epithelial integrity through ferroptosis-mediated oxidative and inflammatory damage. BL effectively suppresses this cascade and protects epithelial junctions, highlighting its therapeutic potential for periodontitis.