Identification of interspecies interactions affecting<i>Porphyromonas gingivalis</i>virulence phenotypes

Tenorio, Elizabeth L; Klein, Brian; Cheung, Wai S.; Hu, Linden T.

doi:10.3402/jom.v3i0.8396

Cited by 20 publications

(15 citation statements)

References 42 publications

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“…The alveolar bone loss levels positively correlated with the severity of periodontal inflammation [29]. In our study, we could observe that all the diabetes mice exhibited alveolar bone loss and db/db mice exhibited more compared to other diabetes mice in both the infection and shame-infection groups.…”

Section: Discussionsupporting

confidence: 53%

Comparison of Experimental Diabetic Periodontitis Induced byPorphyromonas gingivalisin Mice

Wang

Zhang

Aprecio

et al. 2016

Journal of Diabetes Research

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Periodontitis is one of the severe complications in diabetic patients and gingival epithelium plays an initial role on the onset and progression of this disease. However the potential mechanism is yet sufficiently understood. Meanwhile, the research on the correlational experimental animal models was also insufficient. Here, we established periodontitis with type 2 diabetes in db/db and Tallyho/JngJ (TH) mice and periodontitis with type 1 diabetes in streptozotocin induced diabetes C57BL/6J (STZ-C57) mice by oral infection of periodontal pathogen Porphyromonas gingivalis W50. We demonstrated that periodontal infected mice with high blood glucose levels showed dramatically more alveolar bone loss than their counterparts, in which infected db/db mice exhibited the most bone defects. No contrary impact could be observed between this periodontal infection and onset and severity of diabetes. The expressions of PTPN2 were inhibited whereas the expression of JAK1, STAT1, and STAT3 increased dramatically in gingival epithelia and the serum TNF-α also significantly increased in the mice with diabetic periodontitis. Our results indicated that the variations of inflammation-related protein expressions in gingival epithelia might lead to the phenotype differences in the mice with diabetic periodontitis.

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Section: Discussionsupporting

confidence: 53%

Comparison of Experimental Diabetic Periodontitis Induced byPorphyromonas gingivalisin Mice

Wang

Zhang

Aprecio

et al. 2016

Journal of Diabetes Research

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“…The fact that numbers of both bacteria are decreasing in the control can be due to bacterial interactions, in this 6-species model. For example, several strains of A. naeslundii have already been observed to inhibit growth of P. gingivalis [32]. Besides a decrease in the control of P. gingivalis of P. intermedia, it was observed that the concentrations of these two bacteria in the presence of Bdellovibrio did not decrease as much as in the 2-species model, additionally the numbers of S. mitis and A. naeslundii tended to increase slightly.…”

Section: Discussionmentioning

confidence: 94%

Effect of Bdellovibrio bacteriovorus HD100 on multispecies oral communities

et al. 2015

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The predation of Bdellovibrio bacteriovorus on different periodontal pathogens has already been described. However, it is necessary to consider the polymicrobial nature of periodontal disease. The current study explores the predation of Bdellovibrio on oral pathogens organized in multispecies communities. The effect of the predator was evaluated on in vitro six species communities with microbial culturing. Additionally, the effect on ex vivo subgingival plaque and saliva samples from periodontitis patients was assessed. In the latter experiment results were examined with microbial culturing, quantitative polymerase chain reaction (qPCR) and denaturing gradient gel electrophoresis (DGGE). The latter technique was used to get an overview of the whole mixed microbial population. Results showed that even in more complex models, B. bacteriovorus was still able to predate on Fusobacterium nucleatum and Aggregatibacter actinomycetemcomitans. However predation on Prevotella intermedia and Porphyromonas gingivalis could not be validated in multispecies models. The effect of Bdellovibrio was not restricted to the target bacteria. Changes in the overall ecology of the different models were evident. It could be concluded that the efficiency of predation decreased when complexity of the models increased. However, B. bacteriovorus was able to attack two important oral pathogens, F. nucleatum, and A. actinomycetemcomitans, even when present in ex vivo clinical samples. These effects still have to be validated in in vivo models to see the impact of Bdellovibrio on the whole bacterial ecology.

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“…P. gingivalis can coaggregate with a variety of oral bacteria, such as Fusobacterium nucleatum, Actinomyces viscosus, T. denticola, and species of Streptococcus, such as Streptococcus oralis and Streptococcus gordonii (9, 10). There are also negative interactions wherein streptococci inhibit P. gingivalis growth and protease activity (11,12). In a clinical study, Wang et al have shown that there is a negative correlation of distributions of Streptococcus cristatus and P. gingivalis in subgingival plaque (13).…”

mentioning

confidence: 99%

The Periodontal Pathogen Porphyromonas gingivalis Induces Expression of Transposases and Cell Death of Streptococcus mitis in a Biofilm Model

Duran-Pinedo¹,

Baker²,

Frias-Lopez

2014

Infect Immun

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Oral microbial communities are extremely complex biofilms with high numbers of bacterial species interacting with each other (and the host) to maintain homeostasis of the system. Disturbance in the oral microbiome homeostasis can lead to either caries or periodontitis, two of the most common human diseases. Periodontitis is a polymicrobial disease caused by the coordinated action of a complex microbial community, which results in inflammation of tissues that support the teeth. It is the most common cause of tooth loss among adults in the United States, and recent studies have suggested that it may increase the risk for systemic conditions such as cardiovascular diseases. In a recent series of papers, Hajishengallis and coworkers proposed the idea of the "keystone-pathogen" where low-abundance microbial pathogens (Porphyromonas gingivalis) can orchestrate inflammatory disease by turning a benign microbial community into a dysbiotic one. The exact mechanisms by which these pathogens reorganize the healthy oral microbiome are still unknown. In the present manuscript, we present results demonstrating that P. gingivalis induces S. mitis death and DNA fragmentation in an in vitro biofilm system. Moreover, we report here the induction of expression of multiple transposases in a Streptococcus mitis biofilm when the periodontopathogen P. gingivalis is present. Based on these results, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown mechanism, shaping the oral microbiome to its advantage.T he human oral microbiome consists of over 600 individual taxa (1, 2). Its complexity and the fact that a large fraction of species is noncultivable have hampered our knowledge of the molecular and metabolic interactions that occur between the species of the bacterial biofilm and between bacteria and host.Periodontal disease is a polymicrobial inflammatory biofilm-mediated pathology that leads to a progressive loosening and eventual loss of teeth (3, 4), and it is responsible for half of all tooth loss in adults that occurs in moderate form in 39% of American adults and in severe form in 9% of adults. Polymicrobial diseases are increasingly being recognized as more frequent than previously thought (5). In these diseases there are complex interactions among the etiologic agents, which ultimately lead to disease. In the microbial etiology of periodontitis it is generally accepted that a consortium of bacteria, not a single microorganism, is involved in the disease. Nonetheless, it is well established that in destructive periodontitis, the "red complex" (Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia) are key players in the disease process (6).A more holistic treatment of periodontitis or any other polymicrobial disease requires a better understanding of the ecology of the microbial community and the mechanisms that cause the shift from a mature stable biofilm to a dysbiotic community responsible for disease. Maintaining a healthy biofilm would be a less invasive strategy than removing an ...

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Identification of interspecies interactions affectingPorphyromonas gingivalisvirulence phenotypes

Cited by 20 publications

References 42 publications

Comparison of Experimental Diabetic Periodontitis Induced byPorphyromonas gingivalisin Mice

Comparison of Experimental Diabetic Periodontitis Induced byPorphyromonas gingivalisin Mice

Effect of Bdellovibrio bacteriovorus HD100 on multispecies oral communities

The Periodontal Pathogen Porphyromonas gingivalis Induces Expression of Transposases and Cell Death of Streptococcus mitis in a Biofilm Model

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