尼生素是一种益生菌细菌素，可减轻牙周病引发的大脑微生物组失调和类似阿尔茨海默病的神经炎症。

Nisin a probiotic bacteriocin mitigates brain microbiome dysbiosis and Alzheimer's disease-like neuroinflammation triggered by periodontal disease.

机构信息

Department of Orofacial Sciences, School of Dentistry, University of California San Francisco, San Francisco, CA, 94143, USA.

Department of Periodontology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510050, China.

出版信息

J Neuroinflammation. 2023 Oct 6;20(1):228. doi: 10.1186/s12974-023-02915-6.

DOI:10.1186/s12974-023-02915-6

PMID:37803465

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10557354/

Abstract

INTRODUCTION

Periodontitis-related oral microbial dysbiosis is thought to contribute to Alzheimer's disease (AD) neuroinflammation and brain amyloid production. Since probiotics can modulate periodontitis/oral dysbiosis, this study examined the effects of a probiotic/lantibiotic, nisin, in modulating brain pathology triggered by periodontitis.

METHODS

A polymicrobial mouse model of periodontal disease was used to evaluate the effects of this disease on brain microbiome dysbiosis, neuroinflammation, Alzheimer's-related changes, and nisin's therapeutic potential in this context.

RESULTS

16S sequencing and real-time PCR data revealed that Nisin treatment mitigated the changes in the brain microbiome composition, diversity, and community structure, and reduced the levels of periodontal pathogen DNA in the brain induced by periodontal disease. Nisin treatment significantly decreased the mRNA expression of pro-inflammatory cytokines (Interleukin-1β/IL-1 β, Interleukin 6/IL-6, and Tumor Necrosis Factor α/TNF-α) in the brain that were elevated by periodontal infection. In addition, the concentrations of amyloid-β 42 (Aβ42), total Tau, and Tau (pS199) (445.69 ± 120.03, 1420.85 ± 331.40, 137.20 ± 36.01) were significantly higher in the infection group compared to the control group (193.01 ± 31.82, 384.27 ± 363.93, 6.09 ± 10.85), respectively. Nisin treatment markedly reduced the Aβ42 (261.80 ± 52.50), total Tau (865.37 ± 304.93), and phosphorylated Tau (82.53 ± 15.77) deposition in the brain of the infection group.

DISCUSSION

Nisin abrogation of brain microbiome dysbiosis induces beneficial effects on AD-like pathogenic changes and neuroinflammation, and thereby may serve as a potential therapeutic for periodontal-dysbiosis-related AD.

摘要

简介

牙周炎相关的口腔微生物失调被认为有助于阿尔茨海默病（AD）的神经炎症和大脑淀粉样蛋白的产生。由于益生菌可以调节牙周炎/口腔失调，本研究检查了一种益生菌/类抗生素，乳链菌肽，在调节牙周炎引发的大脑病理学中的作用。

方法

使用多微生物牙周炎小鼠模型来评估这种疾病对大脑微生物组失调、神经炎症、与阿尔茨海默病相关的变化以及乳链菌肽在这种情况下的治疗潜力的影响。

结果

16S 测序和实时 PCR 数据显示，乳链菌肽治疗减轻了大脑微生物组组成、多样性和群落结构的变化，并降低了牙周病引起的大脑中牙周病原体 DNA 的水平。乳链菌肽治疗显著降低了由牙周感染引起的大脑中促炎细胞因子（白细胞介素 1β/IL-1β、白细胞介素 6/IL-6 和肿瘤坏死因子α/TNF-α）的 mRNA 表达。此外，淀粉样蛋白-β 42（Aβ42）、总 Tau 和 Tau（pS199）（445.69±120.03、1420.85±331.40、137.20±36.01）的浓度在感染组中明显高于对照组（193.01±31.82、384.27±363.93、6.09±10.85）。乳链菌肽治疗显著降低了感染组大脑中 Aβ42（261.80±52.50）、总 Tau（865.37±304.93）和磷酸化 Tau（82.53±15.77）的沉积。