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Oral Administration of P. gingivalis Induces Dysbiosis of Gut Microbiota and Impaired Barrier Function Leading to Dissemination of Enterobacteria to the Liver

Open access
Nakajima, Mayuka, Arimatsu, Kei, Kato, Tamotsu, Matsuda, Yumi, Minagawa, Takayoshi, Takahashi, Naoki, Ohno, Hiroshi, Yamazaki, Kazuhisa·2015·PLOS ONE

Abstract

Although periodontitis has been implicated as a risk factor for various systemic diseases, the precise mechanisms by which periodontitis induces systemic disease remain to be elucidated. We have previously revealed that repeated oral administration of Porphyromonas gingivalis elicits endotoxemia via changes in the gut microbiota of the ileum, and thereby induces systemic inflammation and insulin resistance. However, it is not clear to what extent a single administration of P. gingivalis could affect gut microbiota composition, gut barrier function, and subsequent influx of gut microbiota into the liver. Therefore, in the present study, C57BL/6 mice were orally administered P. gingivalis (strain W83) once and compared to sham-inoculated mice. The phylogenetic structure and diversity of microbial communities in the gut and liver were analyzed by pyrosequencing the 16S ribosomal RNA genes. Serum endotoxin activity was determined by a Limulus amebocyte lysate test. Gene expression in the intestine and expression of 16S rRNA genes in the blood and liver were examined by quantitative polymerase chain reaction. Administration of P. gingivalis significantly altered gut microbiota, with an increased proportion of phylum Bacteroidetes, a decreased proportion of phylum Firmicutes, and increased serum endotoxin levels. In the intestinal tissues, gene expression of tjp-1 and occludin, which are involved in intestinal permeability, were downregulated. Higher amounts of bacterial DNA were detected in the liver of infected mice. Importantly, changes in gut microbiota preceded systemic inflammatory changes. These results further support the idea that disturbance of the gut microbiota composition by orally derived periodontopathic bacteria may be a causal mechanism linking periodontitis and systemic disease.

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Research works printed but not linked: 20

  1. NG Chávarry, 2009, The relationship between diabetes mellitus and destructive periodontal disease: a meta-analysis, Oral Health Prev Dent, 7, 107
  2. GE Salvi, 2008, Effects of diabetes mellitus on periodontal and peri-implant conditions: update on associations and risks, J Clin Periodontol, 35, 398, 10.1111/j.1600-051X.2008.01282.x · DOI · Paper page
  3. AA Bahekar, 2007, The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis, Am Heart J, 154, 830, 10.1016/j.ahj.2007.06.037 · DOI · Paper page
  4. LL Humphrey, 2008, Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis, J Gen Intern Med, 23, 2079, 10.1007/s11606-008-0787-6 · DOI · Paper page
  5. S Kaur, 2013, Periodontal disease and rheumatoid arthritis: a systematic review, J Dent Res, 92, 399, 10.1177/0022034513483142 · DOI · Paper page
  6. MP Cullinan, 2013, Periodontal disease and systemic illness: will the evidence ever be enough?, Periodontol 2000, 62, 271, 10.1111/prd.12007 · DOI · Paper page
  7. S Fukuda, 2014, Gut microbiome and metabolic diseases, Semin Immunopathol, 36, 103, 10.1007/s00281-013-0399-z · DOI
  8. Z Armingohar, 2014, Bacteria and bacterial DNA in atherosclerotic plaque and aneurysmal wall biopsies from patients with and without periodontitis, J Oral Microbiol, 6, 23408, 10.3402/jom.v6.23408 · DOI
  9. JJ Kozich, 2013, Development of a dual-index sequencing strategy and curation pipeline for analyzing amplicon sequence data on the MiSeq Illumina sequencing platform, Appl Environ Microbiol, 79, 5112, 10.1128/AEM.01043-13 · DOI · Paper page
  10. RC Edgar, 2010, Search and clustering orders of magnitude faster than BLAST, Bioinformatics, 26, 2460, 10.1093/bioinformatics/btq461 · DOI · Paper page
  11. K Boutaga, 2007, Comparison of subgingival bacterial sampling with oral lavage for detection and quantification of periodontal pathogens by real-time polymerase chain reaction, J Periodontol, 78, 79, 10.1902/jop.2007.060078 · DOI
  12. I Saygun, 2011, Salivary infectious agents and periodontal disease status, J Periodontal Res, 46, 235, 10.1111/j.1600-0765.2010.01335.x · DOI · Paper page
  13. B von Troil-Linden, 1995, Salivary levels of suspected periodontal pathogens in relation to periodontal status and treatment, J Dent Res, 74, 1789, 10.1177/00220345950740111201 · DOI
  14. J Wang, 2013, Metagenomic sequencing reveals microbiota and its functional potential associated with periodontal disease, Scientific reports, 3, 1843, 10.1038/srep01843 · DOI · Paper page
  15. PS Kumar, 2006, Changes in periodontal health status are associated with bacterial community shifts as assessed by quantitative 16S cloning and sequencing, J Clin Microbiol, 44, 3665, 10.1128/JCM.00317-06 · DOI · Paper page
  16. BM Brinkman, 2013, Gut microbiota affects sensitivity to acute DSS-induced colitis independently of host genotype, Inflamm Bowel Dis, 19, 2560, 10.1097/MIB.0b013e3182a8759a · DOI
  17. S Rausch, 2013, Small intestinal nematode infection of mice is associated with increased enterobacterial loads alongside the intestinal tract, PLoS One, 8, e74026, 10.1371/journal.pone.0074026 · DOI
  18. C Lozupone, 2012, Identifying genomic and metabolic features that can underlie early successional and opportunistic lifestyles of human gut symbionts, Genome Res, 22, 1974, 10.1101/gr.138198.112 · DOI
  19. ND Vaziri, 2012, Disintegration of colonic epithelial tight junction in uremia: a likely cause of CKD-associated inflammation, Nephrol Dial Transplant, 27, 2686, 10.1093/ndt/gfr624 · DOI · Paper page
  20. PD Cani, 2007, Metabolic endotoxemia initiates obesity and insulin resistance, Diabetes, 56, 1761, 10.2337/db06-1491 · DOI · Paper page

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Metadata

Authors
Nakajima, M., Arimatsu, K., Kato, T., Matsuda, Y., Minagawa, T., Takahashi, N., Ohno, H., & Yamazaki, K.
Venue
PLOS ONE
Published
2015-07-28
Volume
10
Issue
7
Pages
e0134234
ISSN
1932-6203 (ISSN-L)
OpenAlex
W985591008
Cited by
382
References
16
FWCI
7.85
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Oral Administration of P. gingivalis Induces Dysbiosis of Gut Microbiota and Impaired Barrier Function Leading to Dissemination of Enterobacteria to the Liver. https://app.cochat.ai/papers/10.1371/journal.pone.0134234
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Nakajima, M., Arimatsu, K., Kato, T., Matsuda, Y., Minagawa, T., Takahashi, N., Ohno, H., & Yamazaki, K. (2015). Oral Administration of P. gingivalis Induces Dysbiosis of Gut Microbiota and Impaired Barrier Function Leading to Dissemination of Enterobacteria to the Liver. PLOS ONE. https://doi.org/10.1371/journal.pone.0134234

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