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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

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          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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          Immunoglobulin A coating identifies colitogenic bacteria in inflammatory bowel disease.

          Specific members of the intestinal microbiota dramatically affect inflammatory bowel disease (IBD) in mice. In humans, however, identifying bacteria that preferentially affect disease susceptibility and severity remains a major challenge. Here, we used flow-cytometry-based bacterial cell sorting and 16S sequencing to characterize taxa-specific coating of the intestinal microbiota with immunoglobulin A (IgA-SEQ) and show that high IgA coating uniquely identifies colitogenic intestinal bacteria in a mouse model of microbiota-driven colitis. We then used IgA-SEQ and extensive anaerobic culturing of fecal bacteria from IBD patients to create personalized disease-associated gut microbiota culture collections with predefined levels of IgA coating. Using these collections, we found that intestinal bacteria selected on the basis of high coating with IgA conferred dramatic susceptibility to colitis in germ-free mice. Thus, our studies suggest that IgA coating identifies inflammatory commensals that preferentially drive intestinal disease. Targeted elimination of such bacteria may reduce, reverse, or even prevent disease development. Copyright © 2014 Elsevier Inc. All rights reserved.
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            Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis.

            Periodontal disease is common among adults in the US and is a potential source of chronic inflammation. Recent data have suggested an important role for chronic inflammation in the development of coronary heart disease (CHD). To aid the United States Preventive Services Task Force (USPSTF) in evaluating whether periodontal disease is an independent novel risk factor for incident CHD. Studies were identified by searching Medline (1966 through March 2008) and reviewing prior systematic reviews, reference lists, and consulting experts. Prospective cohort studies that assessed periodontal disease, Framingham risk factors, and coronary heart disease incidence in the general adult population without known CHD were reviewed and quality rated using criteria developed by the USPSTF. Meta-analysis of good and fair quality studies was conducted to determine summary estimates of the risk of CHD events associated with various categories of periodontal disease. We identified seven articles of good or fair quality from seven cohorts. Several studies found periodontal disease to be independently associated with increased risk of CHD. Summary relative risk estimates for different categories of periodontal disease (including periodontitis, tooth loss, gingivitis, and bone loss) ranged from 1.24 (95% CI 1.01-1.51) to 1.34 (95% CI 1.10-1.63). Risk estimates were similar in subgroup analyses by gender, outcome, study quality, and method of periodontal disease assessment. Periodontal disease is a risk factor or marker for CHD that is independent of traditional CHD risk factors, including socioeconomic status. Further research in this important area of public health is warranted.
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              The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis.

              Previous studies have shown conflicting results as to whether periodontitis (PD) is associated with increased risk of coronary heart disease (CHD). The aim of the current study was to evaluate whether such an association exists. A systematic review of the literature revealed 5 prospective cohort studies (follow-up >6 years), 5 case-control studies, and 5 cross-sectional studies that were eligible for meta-analysis. Individual studies were adjusted for confounding factors such as age, sex, diabetes mellitus, and smoking. The 3 study categories were analyzed separately. Heterogeneity of the studies was assessed by Cochran Q test. The studies were homogeneous; therefore, the Mantel-Haenszel fixed-effect model was used to compute common relative risk and odds ratio (OR). Meta-analysis of the 5 prospective cohort studies (86092 patients) indicated that individuals with PD had a 1.14 times higher risk of developing CHD than the controls (relative risk 1.14, 95% CI 1.074-1.213, P < .001). The case-control studies (1423 patients) showed an even greater risk of developing CHD (OR 2.22, 95% CI 1.59-3.117, P < .001). The prevalence of CHD in the cross-sectional studies (17724 patients) was significantly greater among individuals with PD than in those without PD (OR 1.59, 95% CI 1.329-1.907, P < .001). When the relationship between number of teeth and incidence of CHD was analyzed, cohort studies showed 1.24 times increased risk (95% CI 1.14-1.36, P < .0001) of development of CHD in patients with <10 teeth. This meta-analysis indicates that both the prevalence and incidence of CHD are significantly increased in PD. Therefore, PD may be a risk factor for CHD. Prospective studies are required to prove this assumption and evaluate risk reduction with the treatment of PD.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                28 July 2015
                2015
                : 10
                : 7
                : e0134234
                Affiliations
                [1 ]Laboratory of Periodontology and Immunology, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
                [2 ]Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
                [3 ]Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Japan
                [4 ]CREST, Japan Science and Technology Agency, Kawaguchi, Japan
                GI Lab, UNITED STATES
                Author notes

                Competing Interests: K. Yamazaki received a grant from SUNSTAR Inc. but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials. No further competing interests exist.

                Conceived and designed the experiments: KY HO. Performed the experiments: MN KA TK YM TM NT. Analyzed the data: MN TK KY. Contributed reagents/materials/analysis tools: TK HO. Wrote the paper: MN TK KY.

                Article
                PONE-D-15-15324
                10.1371/journal.pone.0134234
                4517782
                26218067
                590a19b1-e7f4-4f54-97ea-5edd8270c73a
                Copyright @ 2015

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                : 13 April 2015
                : 7 July 2015
                Page count
                Figures: 6, Tables: 0, Pages: 15
                Funding
                This work was supported by the Japan Society for the Promotion of Science KAKENHI 23390476, 25670882, and 15H02578 (KY); The Japan Science and Technology Agency (HO); and Sunstar Inc. (KY). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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