益生菌鼠李糖乳杆菌GG可预防牙龈卟啉单胞菌和具核梭杆菌引起的肠道菌群失调。
Probiotic Lactobacillus Rhamnosus GG Protects Against P. Gingivalis And F. Nucleatum Gut Dysbiosis.
作者信息
Gatej Simona M, Bright Richard, Weyrich Laura S, Marino Victor, Christophersen Claus T, Gibson Rachel J, Gully Neville, Zilm Peter, Bartold P Mark
机构信息
Faculty of Health and Medical Sciences, Adelaide Dental School, The University of Adelaide, Adelaide, South Australia, Australia. Email
Faculty of Health and Medical Sciences, Adelaide Dental School, The University of Adelaide, Adelaide, South Australia, Australia.
出版信息
J Int Acad Periodontol. 2020 Apr 1;22(2):18-27.
OBJECTIVES
This study investigated changes induced by Porphyromonas gingivalis and on gastrointestinal histology and gut microbiome in a mouse model of experimental periodontitis. The effect of probiotic Lactobacillus rhamnosus GG (LGG) in altering these changes was also investigated.
METHODS
IThirty-six mice were allocated into six groups. Experimental alveolar bone loss was induced by oral inoculation with P. gingivalis and F. nucleatum. LGG was orally inoculated or orally gavaged. Gastrointestinal tissue changes were assessed using histological analysis and immunohistochemistry. Caecal microbiome was analysed by sequencing 16S rRNA genes of caecal content.
RESULTS
Inoculation with P. gingivalis and F. nucleatum induced inflammation throughout gastrointestinal tract (p less than 0.05), increased expression of IL-6 in ileum (p = 0.052) and altered composition of caecal microbiome (p less than 0.05) in experimental mice compared to controls. Mice treated with LGG had reduced tissue inflammation in duodenum (p = 0.044) and lowered levels of IL-6 in ileum (p = 0.048) when compared with disease. LGG therapy influenced gut microbiome changes.
CONCLUSION
P. gingivalis and F. nucleatum inoculation induced significant changes in intestinal inflammation and caecal microbiome. Oral gavage with LGG exerted a protective effect against intestinal inflammation and limited gut microbiome changes associated with P. gingivalis and F. nucleatum.
目的
本研究在实验性牙周炎小鼠模型中，探究牙龈卟啉单胞菌诱导的变化及其对胃肠道组织学和肠道微生物群的影响。同时也研究了益生菌鼠李糖乳杆菌GG（LGG）对改变这些变化的作用。
方法
将36只小鼠分为六组。通过口服接种牙龈卟啉单胞菌和具核梭杆菌诱导实验性牙槽骨丧失。对小鼠进行LGG口服接种或灌胃。使用组织学分析和免疫组织化学评估胃肠道组织变化。通过对盲肠内容物的16S rRNA基因进行测序分析盲肠微生物群。
结果
与对照组相比，接种牙龈卟啉单胞菌和具核梭杆菌可诱导实验小鼠整个胃肠道发生炎症（p<0.05），回肠中白细胞介素-6（IL-6）表达增加（p = 0.052），盲肠微生物群组成改变（p<0.05）。与患病小鼠相比，接受LGG治疗的小鼠十二指肠组织炎症减轻（p = 0.044），回肠中IL-6水平降低（p = 0.048）。LGG治疗影响肠道微生物群的变化。
结论
接种牙龈卟啉单胞菌和具核梭杆菌可引起肠道炎症和盲肠微生物群的显著变化。口服LGG对肠道炎症具有保护作用，并限制了与牙龈卟啉单胞菌和具核梭杆菌相关的肠道微生物群变化。
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