Endotoxemia by Porphyromonas gingivalis Injection Aggravates Non-alcoholic Fatty Liver Disease, Disrupts Glucose/Lipid Metabolism, and Alters Gut Microbiota in Mice

Sasaki, Naoki; Katagiri, Seiji; Komazaki, Rina; Watanabe, Kouichi; Maekawa, Shogo; Shiba, Takahiko; Udagawa, Sayuri; Takeuchi, Yasuo; Ohtsu, Anri; Kohda, Takashi; Tohara, Haruka; Matsuda, Naoyuki; Hirota, Tomomitsu; Tamari, Mayumi; Izumi, Yuichi

doi:10.3389/fmicb.2018.02470

Cited by 60 publications

(83 citation statements)

References 56 publications

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“…The relationship between periodontitis and NAFLD has attracted wide public concern recently (Akinkugbe et al, 2017;Sasaki et al, 2018;Tomofuji et al, 2007Tomofuji et al, , 2009. Yoneda et al (Yoneda et al, 2012) have found that the prevalence of P. gingivalis infection was significantly higher in the NAFLD patients compared to the healthy subjects, and periodontal treatments may improve the condition of NAFLD of which have periodontitis.…”

Section: Discussionmentioning

confidence: 99%

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

et al. 2020

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Periodontitis is an inflammatory oral disease characterized by periodontal pathogenic bacteria as the initiating factor and the destruction of periodontal supporting tissues, that are gingiva, periodontal membrane, and alveolar bone resorption (Kinane, Stathopoulou, & Papapanou, 2017), affecting most of the adults worldwide (Bellentani, 2017; Eke et al., 2015). One of the pathogenic factors of periodontitis is imbalance in the host reactions caused by the appearance and persistence of dysbiotic oral microbiota and other metabolites that cause the overproduction of inflammatory mediators. In addition, periodontitis can induce an imbalance between oxidant and antioxidant agents, ultimately causes the periodontal tissue damages (Hajishengallis, 2015).

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Section: Discussionmentioning

confidence: 99%

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

et al. 2020

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“…Systemic metabolic disorders may allow new infection from the oral cavity and lead to a further serious condition. We have reported that oral administration of periodontopathic bacteria in mice with high‐fat diet affected glucose/lipid metabolism and aggravated non‐alcoholic fatty liver disease (Komazaki et al, ; Sasaki et al, ). However, Blasco‐Baque et al reported that insulin resistance in the high‐fat fed mouse was enhanced by periodontitis caused by alteration of three periodontopathic bacteria in the oral cavity without mainly affecting gut microbiota (Blasco‐Baque et al, ).…”

Section: Discussionmentioning

confidence: 99%

Influence of Porphyromonas gingivalis in gut microbiota of streptozotocin‐induced diabetic mice

et al. 2019

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Objectives Increasing evidence suggests that periodontitis can exacerbate diabetes, and gut bacterial dysbiosis appears to be linked with the diabetic condition. The present study examined the effects of oral administration of the periodontopathic bacterium, Porphyromonas gingivalis, on the gut microbiota and systemic conditions in streptozotocin‐induced diabetic mice. Materials and Methods Diabetes was induced by streptozotocin injection in C57BL/6J male mice (STZ). STZ and wild‐type (WT) mice were orally administered P. gingivalis (STZPg, WTPg) or saline (STZco, WTco). Feces were collected, and the gut microbiome was examined by 16S rRNA gene sequencing. The expression of genes related to inflammation, epithelial tight junctions, and glucose/fatty acid metabolism in the ileum or liver were examined by quantitative PCR. Results The relative abundance of several genera, including Brevibacterium, Corynebacterium, and Facklamia, was significantly increased in STZco mice compared to WTco mice. The relative abundances of Staphylococcus and Turicibacter in the gut microbiome were altered by oral administration of P. gingivalis in STZ mice. STZPg mice showed higher concentrations of fasting blood glucose and inflammatory genes levels in the ileum, compared to STZco mice. Conclusions Oral administration of P. gingivalis altered the gut microbiota and aggravated glycemic control in streptozotocin‐induced diabetic mice.

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“…DNA extracted from saliva, and feces samples were purified and used to generate a multiplexed amplicon library (16S rDNA V3-V4 region) as previously described (Komazaki et al, 2017;Sasaki et al, 2018). The MiSeq platform (Illumina, San Diego, CA, USA) was used to generate 250-bp paired-end sequences.…”

Section: S Rrna Gene Sequencing and Data Processingmentioning

confidence: 99%

Re-initiation of Oral Food Intake Following Enteral Nutrition Alters Oral and Gut Microbiota Communities

Katagiri

Shiba

Tohara

et al. 2019

Front. Cell. Infect. Microbiol.

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Stroke is associated with multiple forms of disability, including dysphagia. Post-stroke dysphagia increases the risks of pneumonia and mortality and often results in cessation of oral feeding. However, appropriate rehabilitation methods can eventually lead to resumption of oral food intake. This study tried to clarify that re-initiating oral food intake could modify the composition of oral/gut microbial communities in patients with dysphagia. From 78 patients with sub-acute stage of stroke, 11 complete tube feeding subjects without taking antibiotics were enrolled and received rehabilitation for re-initiation of oral food intake, and 8 subjects were brought back to complete oral feeding. Oral and gut microbiota community profiles were evaluated using 16S rRNA sequencing of the saliva and feces samples before and after re-initiation of oral food intake in patients recovering from enteral nutrition under the same nutrient condition. Standard nutrition in the hospital was 1,840 kcal, including protein = 75 g, fat = 45 g, and carbohydrates = 280 g both for tube and oral feeding subjects. Oral food intake increased oral and gut microbiome diversity and altered the composition of the microbiome. Oral and gut microbiome compositions were drastically different; however, the abundance of family Carnobacteriaceae and genus Granulicatella was increased in both the oral and gut microbiome after re-initiation of oral food intake. Although oral microbiota showed more significant changes than the gut microbiota, metagenome prediction revealed the presence of more differentially enriched pathways in the gut. In addition, simpler co-occurrence networks of oral and gut microbiomes, indicating improved dysbiosis of the microbiome, were observed during oral feeding as compared to that during tube feeding. Oral food intake affects oral and gut microbiomes in patients recovering from enteral nutrition. Rehabilitation for dysphagia can modify systemic health by increasing the diversity and altering the composition and co-occurrence network structure of oral and gut microbial communities.

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Endotoxemia by Porphyromonas gingivalis Injection Aggravates Non-alcoholic Fatty Liver Disease, Disrupts Glucose/Lipid Metabolism, and Alters Gut Microbiota in Mice

Cited by 60 publications

References 56 publications

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

Influence of Porphyromonas gingivalis in gut microbiota of streptozotocin‐induced diabetic mice

Re-initiation of Oral Food Intake Following Enteral Nutrition Alters Oral and Gut Microbiota Communities

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