Department of Microbiology and Immunology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Canadian Centre for Human Microbiome and Probiotic Research, Lawson Health Research Institute, London, ON, Canada.
BMC Oral Health. 2021 May 7;21(1):245. doi: 10.1186/s12903-021-01606-z.
Periodontal disease represents a major health concern. The administration of beneficial microbes has been increasing in popularity over efforts to manipulate the microbes using antimicrobial agents. This study determined the ability of Streptococcus salivarius to inhibit IL-6 and IL-8 production by gingival fibroblasts when activated by periodontal pathogens and their effect on the salivary microbiome.
Primary human gingival fibroblasts were challenged with Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Fusobacterium nucleatum and a combination of all three. IL-6 and IL-8 cytokine release were measured. Using this same model, S. salivarius K12, M18 and different supernatant and whole-cell lysate fractions of S. salivarius K12 were administered to pathogen-induced fibroblasts. A patient study of healthy participants was also conducted to determine the effect S. salivarius K12 had on the native microbiome using 16S next generation sequence analysis.
All pathogens tested induced a significant IL-6 and IL-8 response. S. salivarius K12 or M18, did not exhibit an increase in inflammatory cytokines. When either of the probiotic strains were co-administered with a pathogen, there were significant reductions in both IL-6 and IL-8 release. This effect was also observed when gingival fibroblasts were pre-treated with either S. salivarius K12 or M18 and then stimulated with the oral pathogens. Chewing gum containing S. salivarius K12 did not alter the salivary microbiome and did not increase inflammatory markers in the oral cavity.
S. salivarius K12 and M18 prevented immune activation induced by periodontal disease pathogens. S. salivarius K12 did not alter the salivary microbiome or induce immune activation when administered as a chewing gum. These results warrant further study to determine if it may be an effective treatment in a model of periodontal disease.
牙周病是一个主要的健康问题。有益微生物的管理越来越受到重视，而不是使用抗菌剂来操纵微生物。本研究旨在确定唾液链球菌（Streptococcus salivarius）在被牙周病病原体激活时抑制牙龈成纤维细胞产生白细胞介素 6（IL-6）和白细胞介素 8（IL-8）的能力，以及其对唾液微生物组的影响。
原代人牙龈成纤维细胞分别受到牙龈卟啉单胞菌（Porphyromonas gingivalis）、伴放线放线杆菌（Aggregatibacter actinomycetemcomitans）和核梭杆菌（Fusobacterium nucleatum）以及三者的组合刺激。测量白细胞介素 6 和白细胞介素 8 细胞因子的释放。在相同的模型中，向病原体诱导的成纤维细胞中添加唾液链球菌（Streptococcus salivarius）K12、M18 以及唾液链球菌（Streptococcus salivarius）K12 的不同上清液和全细胞裂解液。还对健康参与者进行了一项患者研究，通过 16S 下一代测序分析，确定唾液链球菌（Streptococcus salivarius）K12 对天然微生物组的影响。
所有测试的病原体都诱导了显著的 IL-6 和 IL-8 反应。唾液链球菌（Streptococcus salivarius）K12 或 M18 没有表现出炎症细胞因子的增加。当两种益生菌菌株与病原体一起给药时，IL-6 和 IL-8 的释放均显著减少。当牙龈成纤维细胞先用唾液链球菌（Streptococcus salivarius）K12 或 M18 预处理，然后用口腔病原体刺激时，也观察到了这种效果。含有唾液链球菌（Streptococcus salivarius）K12 的口香糖不会改变唾液微生物组，也不会增加口腔中的炎症标志物。
唾液链球菌（Streptococcus salivarius）K12 和 M18 可阻止牙周病病原体引起的免疫激活。当作为口香糖给药时，唾液链球菌（Streptococcus salivarius）K12 不会改变唾液微生物组或诱导免疫激活。这些结果值得进一步研究，以确定它是否可以成为牙周病模型中的有效治疗方法。
