AUTHOR=Shimabukuro Natali , Cataruci Amália C. de S. , Ishikawa Karin H. , Oliveira Bruna E. de , 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. 

TITLE=Bifidobacterium Strains Present Distinct Effects on the Control of Alveolar Bone Loss in a Periodontitis Experimental Model

JOURNAL=Frontiers in Pharmacology

VOLUME=12

YEAR=2021

URL=https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2021.713595

DOI=10.3389/fphar.2021.713595

ISSN=1663-9812

ABSTRACT=<p>Periodontitis is an inflammatory disease induced by a dysbiotic oral microbiome. Probiotics of the genus <italic>Bifidobacterium</italic> may restore the symbiotic microbiome and modulate the immune response, leading to periodontitis control. We evaluated the effect of two strains of <italic>Bifidobacterium</italic> able to inhibit <italic>Porphyromonas gingivalis</italic> 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. <italic>B. bifidum</italic> 162<sup>2A</sup> [B+ (1622)] and <italic>B. breve</italic> 110<sup>1A</sup> [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 <italic>P. gingivalis</italic> 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. <italic>B. bifidum</italic> 162<sup>2A</sup>, but not <italic>B. breve</italic> 110<sup>1A</sup>, controlled bone destruction in P+ mice. <italic>B. breve</italic> 110<sup>1A</sup> upregulated transcription of <italic>Il-1β</italic>, <italic>Tnf-α</italic>, <italic>Tlr2</italic>, <italic>Tlr4</italic>, and <italic>Nlrp3</italic> in P-B+(1101), which was attenuated by the microbial consortium [P + B+(1101)]. All treatments downregulated transcription of <italic>Il-17</italic>, although treatment with <italic>B. breve</italic> 110<sup>1A</sup> did not yield such low levels of transcripts as seen for the other groups. <italic>B. breve</italic> 110<sup>1A</sup> 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 <italic>Bifidobacterium</italic> is not a common trait of this genus, since <italic>B. breve</italic> 110<sup>1A</sup> induced an inflammatory profile in gingival tissues and did not prevent alveolar bone loss. However, the properties of <italic>B. bifidum</italic> 162<sup>2A</sup> suggest its potential to control periodontitis.</p>