Shimabukuro Natali, Cataruci Amália C de S, Ishikawa Karin H, de Oliveira Bruna E, Kawamoto Dione, Ando-Suguimoto Ellen S, Albuquerque-Souza Emmanuel, Nicoli Jacques R, Ferreira Caroline M, de Lima Jean, Bueno Manuela R, da Silva Leandro B R, Silva Pedro H F, Messora Michel R, Camara Niels O S, Simionato Maria Regina L, Mayer Marcia P A
Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Division of Periodontics, Department of Stomatology, School of Dentistry, University of São Paulo, São Paulo, Brazil.
Front Pharmacol. 2021 Sep 24;12:713595. doi: 10.3389/fphar.2021.713595. eCollection 2021.
Periodontitis is an inflammatory disease induced by a dysbiotic oral microbiome. Probiotics of the genus may restore the symbiotic microbiome and modulate the immune response, leading to periodontitis control. We evaluated the effect of two strains of able to inhibit interaction with host cells and biofilm formation, but with distinct immunomodulatory properties, in a mice periodontitis model. Experimental periodontitis (P+) was induced in C57Bl/6 mice by a microbial consortium of human oral organisms. 162 [B+ (1622)] and 110 [B+ (1101)] were orally inoculated for 45 days. Alveolar bone loss and inflammatory response in gingival tissues were determined. The microbial consortium induced alveolar bone loss in positive control (P + B-), as demonstrated by microtomography analysis, although was undetected in oral biofilms at the end of the experimental period. TNF-α and IL-10 serum levels, and Treg and Th17 populations in gingiva of SHAM and P + B- groups did not differ. 162, but not 110, controlled bone destruction in P+ mice. 110 upregulated transcription of , , , , and in P-B+(1101), which was attenuated by the microbial consortium [P + B+(1101)]. All treatments downregulated transcription of , although treatment with 110 did not yield such low levels of transcripts as seen for the other groups. 110 increased Th17 population in gingival tissues [P-B+ (1101) and P + B+ (1101)] compared to SHAM and P + B-. Administration of both bifidobacteria resulted in serum IL-10 decreased levels. Our data indicated that the beneficial effect of is not a common trait of this genus, since 110 induced an inflammatory profile in gingival tissues and did not prevent alveolar bone loss. However, the properties of 162 suggest its potential to control periodontitis.
牙周炎是一种由口腔微生物群落失调引起的炎症性疾病。该属的益生菌可能会恢复共生微生物群落并调节免疫反应,从而控制牙周炎。我们在小鼠牙周炎模型中评估了两株能够抑制与宿主细胞相互作用和生物膜形成,但具有不同免疫调节特性的该属菌株的效果。通过人类口腔微生物组成的微生物联合体在C57Bl/6小鼠中诱导实验性牙周炎(P+)。将162 [B+ (1622)] 和110 [B+ (1101)] 口服接种45天。测定牙槽骨丢失和牙龈组织中的炎症反应。如显微断层扫描分析所示,微生物联合体在阳性对照(P + B-)中诱导了牙槽骨丢失,尽管在实验期结束时口腔生物膜中未检测到该联合体。假手术组和P + B-组的血清TNF-α和IL-10水平以及牙龈中的调节性T细胞和辅助性T细胞17亚群没有差异。162能够控制P+小鼠的骨破坏,而110则不能。110上调了P-B+(1101)中、、、和的转录,而微生物联合体[P + B+(1101)]减弱了这种上调。所有处理均下调了的转录,尽管用110处理并未产生与其他组一样低水平的转录本。与假手术组和P + B-相比,110增加了牙龈组织中的辅助性T细胞17亚群[P-B+ (1101)和P + B+ (1101)]。两种双歧杆菌的施用均导致血清IL-10水平降低。我们的数据表明,该属的有益作用并非该属的共同特征,因为110在牙龈组织中诱导了炎症特征且未预防牙槽骨丢失。然而,162的特性表明其具有控制牙周炎的潜力。