4.7 Article

Akkermansia muciniphila inhibited the periodontitis caused by Fusobacterium nucleatum

Journal

NPJ BIOFILMS AND MICROBIOMES
Volume 9, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41522-023-00417-0

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Periodontitis, caused by plaque biofilm, is the leading cause of tooth loss in adults and is associated with systemic diseases. Fusobacterium nucleatum plays a role in periodontitis through its virulence factors and coaggregating effects with other periodontal pathogens. Traditional periodontal treatment is time-consuming and expensive, while antibiotic use may lead to oral microbial resistance. Akkermansia muciniphila, a probiotic, can regulate microbial balance and is inversely correlated with various diseases. Co-culture experiments showed that A. muciniphila inhibited the expression of F. nucleatum's virulence gene. Inflammatory effects of F. nucleatum on gingival epithelial cells were inhibited by A. muciniphila through modulation of the TLR/MyD88/NF-kappaB pathway and secretion of inflammatory factors. Animal experiments demonstrated the inhibition of F. nucleatum-induced periodontitis by A. muciniphila in mice.
Periodontitis is the most important cause of tooth loss in adults and is closely related to various systemic diseases. Its etiologic factor is plaque biofilm, and the primary treatment modality is plaque control. Studies have confirmed that Fusobacterium nucleatum can cause periodontitis through its virulence factors and copolymerizing effects with other periodontal pathogens, such as the red complex. Inhibiting F. nucleatum is an essential target for preventing periodontitis. The time-consuming and costly traditional periodontal treatment, periodontal scaling, and root planing are a significant burden on individual and public health. Antibiotic use may lead to oral microbial resistance and microbiome imbalance, while probiotics regulate microbial balance. Akkermansia muciniphila is a critical probiotic isolated from the human intestine. It can protect the integrity of the epithelial barrier, regulate and maintain flora homeostasis, improve metabolism, and colonize the oral cavity. Its abundance is inversely correlated with various diseases. We hypothesized that A. muciniphila could inhibit the effects of F. nucleatum and alleviate periodontitis. Bacterial co-culture experiments showed that A. muciniphila could inhibit the expression of the virulence gene of F. nucleatum. After treating gingival epithelial cells (GECs) with F. nucleatum and A. muciniphila, transcriptome sequencing and ELISA experiments on medium supernatant showed that A. muciniphila inhibited the inflammatory effect of F. nucleatum on GECs by inhibiting TLR/MyD88/NF-& kappa;B pathway modulation and secretion of inflammatory factors. Finally, animal experiments demonstrated that A. muciniphila could inhibit F. nucleatum-induced periodontitis in BALB/c mice.

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