Porphyromonas gingivalis inhibits the release of CXCL8 by gingival epithelial cells and reduces their proliferation. We previously reported that Bifidocaterium sp. and Lactobacillus sp. immunomodulate gingival epithelial cells response to this periodontal pathogen, but their effects on re-epithelialization properties are still unknown. Herein we explored these activities of potential probiotics on gingival epithelial cells and clarified their mechanisms. The immortalized OBA-9 lineage was used to perform in vitro scratches. Twelve clinical isolates and commercially available strains of Bifidobacterium sp. and Lactobacillus sp. were screened. L. casei 324 m and B. pseudolongum 119^1A were selected to perform mechanistic assays with P. gingivalis W83 infection and the following parameters were measured: percentage of re-epithelialization by DAPI immunofluorescence area measurement; cell number by Trypan Blue exclusion assay; CXCL8 regulation by ELISA and RT-qPCR; and expression of CXCL8 cognate receptors-CXCR1 and CXCR2 by Flow Cytometry. Complementary mechanistic assays were performed with CXCL8, in the presence or absence of the CXCR1/CXCR2 inhibitor-reparixin. L. casei 324 m and B. pseudolongum 119^1A enhanced re-epithelialization/cell proliferation as well as inhibited the harmful effects of P. gingivalis W83 on these activities through an increase in the expression and release of CXCL8 and in the number of cells positive for CXCR1/CXCR2. Further, we revealed that the beneficial effects of these potential probiotics were dependent on activation of the CXCL8-CXCR1/CXCR2 axis. The current findings indicate that these potential probiotics strains may improve wound healing in the context of the periodontal tissues by a CXCL8 dependent mechanism.

牙龈卟啉单胞菌抑制牙龈上皮细胞释放 CXCL8 并减少其增殖。我们之前曾报道过Bifidocaterium sp。和乳酸杆菌属。免疫调节牙龈上皮细胞对这种牙周病原体的反应，但它们对再上皮化特性的影响仍然未知。在此，我们探讨了潜在益生菌对牙龈上皮细胞的这些活性，并阐明了它们的机制。永生化的 OBA-9 谱系用于进行体外划痕。双歧杆菌属的十二种临床分离株和市售菌株。和乳酸杆菌属。被筛选。L. casei 324 m 和选择B. pseudolongum 119 ^1A对P. gingivalis W83 感染进行机械测定，并测量以下参数： DAPI 免疫荧光面积测量的再上皮化百分比；通过台盼蓝排除法测定细胞数；通过 ELISA 和 RT-qPCR 调节 CXCL8；通过流式细胞术表达 CXCL8 同源受体-CXCR1 和 CXCR2。在存在或不存在 CXCR1/CXCR2 抑制剂-reparixin 的情况下，用 CXCL8 进行了补充机械分析。L. casei 324 m 和B. pseudolongum 119 ^1A增强再上皮化/细胞增殖并抑制P. gingivalis的有害影响W83 通过增加 CXCL8 的表达和释放以及 CXCR1/CXCR2 阳性细胞数量来了解这些活性。此外，我们发现这些潜在益生菌的有益作用取决于 CXCL8-CXCR1/CXCR2 轴的激活。目前的研究结果表明，这些潜在的益生菌菌株可能通过 CXCL8 依赖性机制改善牙周组织中的伤口愈合。