Filifactor alocis – a new emerging periodontal pathogen

Aruni, Wilson; Mishra, Ashish Kumar; Dou, Youjun; Chioma, O.S.; Hamilton, Brittany N.; Fletcher, Hansel M.

doi:10.1016/j.micinf.2015.03.011

Cited by 93 publications

(98 citation statements)

References 58 publications

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“…The ETF + dehydrogenase complex was also observed in oral pathogens like Porphyromonas gingivalis and Filifactor alocis . These pathogens lead to butyrate production in oral cavity which, as discussed earlier, is cytotoxic in this environment and may lead to disorders like periodontitis (Socransky et al, 1998; Tsuda et al, 2010; Chang et al, 2013; Aruni et al, 2015). Apart from these bacteria residing in human microbiome, a few strains of Azotobacter vinelandii , a bacteria known to thrive in soil environment and those of the thermophillic Thermoanaerobacteria were observed to possess all three subunits of Bcd, which is in line with earlier studies (Ueno et al, 2006).…”

Section: Resultsmentioning

confidence: 96%

“…These butyrogenic oral pathogens include Fusobacterium nucleatum (discussed earlier in this manuscript) which primarily utilizes amino acid metabolism for butyrate production (Jorth et al, 2014). Additionally, other oral pathogenic bacteria like Porphyromonas gingivalis, Tannerella forsythia and Filifactor alocis have also been shown to possess butyrate production pathways (Socransky et al, 1998; Darveau, 2010; Aruni et al, 2015). Our study revealed that while all strains of Porphyromonas gingivalis possessed the Pyruvate, 4-aminobutyrate and Lysine pathways for butyrate production, Filifactor alocis contained Pyruvate and Glutarate pathways and Tannerella forsythia possessed the 4-Aminobutyrate pathway for butyrate production.…”

Section: Resultsmentioning

confidence: 99%

“…Further, it has been implicated in apoptosis and autophagic cell death in gingival cells (Ohkawara et al, 2005). The dysbiosis within oral microbiome is often associated with an increase in butyrate producing pathogens like Porphyromonas gingivalis, Filifactor alocis , and Tannerella forsythia and has also been implicated in diseased conditions like periodontitis (Corpet et al, 1995; Socransky et al, 1998; Aruni et al, 2015). Thus, while butyrate is a beneficial metabolite for gut cells, its presence is likely to show deleterious effects in oral cavity.…”

Section: Introductionmentioning

confidence: 99%

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Comparative In silico Analysis of Butyrate Production Pathways in Gut Commensals and Pathogens

2016

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Biosynthesis of butyrate by commensal bacteria plays a crucial role in maintenance of human gut health while dysbiosis in gut microbiome has been linked to several enteric disorders. Contrastingly, butyrate shows cytotoxic effects in patients with oral diseases like periodontal infections and oral cancer. In addition to these host associations, few syntrophic bacteria couple butyrate degradation with sulfate reduction and methane production. Thus, it becomes imperative to understand the distribution of butyrate metabolism pathways and delineate differences in substrate utilization between pathogens and commensals. The bacteria utilize four pathways for butyrate production with different initial substrates (Pyruvate, 4-aminobutyrate, Glutarate and Lysine) which follow a polyphyletic distribution. A comprehensive mining of complete/draft bacterial genomes indicated conserved juxtaposed genomic arrangement in all these pathways. This gene context information was utilized for an accurate annotation of butyrate production pathways in bacterial genomes. Interestingly, our analysis showed that inspite of a beneficial impact of butyrate in gut, not only commensals, but a few gut pathogens also possess butyrogenic pathways. The results further illustrated that all the gut commensal bacteria (Faecalibacterium, Roseburia, Butyrivibrio, and commensal species of Clostridia etc) ferment pyruvate for butyrate production. On the contrary, the butyrogenic gut pathogen Fusobacterium utilizes different amino acid metabolism pathways like those for Glutamate (4-aminobutyrate and Glutarate) and Lysine for butyrogenesis which leads to a concomitant release of harmful by-products like ammonia in the process. The findings in this study indicate that commensals and pathogens in gut have divergently evolved to produce butyrate using distinct pathways. No such evolutionary selection was observed in oral pathogens (Porphyromonas and Filifactor) which showed presence of pyruvate as well as amino acid fermenting pathways which might be because the final product butyrate is itself known to be cytotoxic in oral diseases. This differential utilization of butyrogenic pathways in gut pathogens and commensals has an enormous ecological impact taking into consideration the immense influence of butyrate on different disorders in humans. The results of this study can potentially guide bioengineering experiments to design therapeutics/probiotics by manipulation of butyrate biosynthesis gene clusters in bacteria.

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Section: Resultsmentioning

confidence: 96%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparative In silico Analysis of Butyrate Production Pathways in Gut Commensals and Pathogens

2016

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“…We then queried the models to identify the predicted microbes and reactions involved in hydrogen sulfide production. The models predicted that Fusobacterium nucleatum , Clostridium perfringens, and Filifactor alocis (formerly Fusobacterium alocis [62]) were significant hydrogen sulfide producers. Moreover, B. fragilis was observed to uptake and utilize this microbially-produced hydrogen sulfide in the models.…”

Section: Resultsmentioning

confidence: 99%

Synthesis of multi-omic data and community metabolic models reveals insights into the role of hydrogen sulfide in colon cancer

Hale

Jeraldo

Mundy

et al. 2018

Methods

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Multi-omic data and genome-scale microbial metabolic models have allowed us to examine microbial communities, community function, and interactions in ways that were not available to us historically. Now, one of our biggest challenges is determining how to integrate data and maximize data potential. Our study demonstrates one way in which to test a hypothesis by combining multi-omic data and community metabolic models. Specifically, we assess hydrogen sulfide production in colorectal cancer based on stool, mucosa, and tissue samples collected on and off the tumor site within the same individuals. 16S rRNA microbial community and abundance data were used to select and inform the metabolic models. We then used MICOM, an open source platform, to track the metabolic flux of hydrogen sulfide through a defined microbial community that either represented on-tumor or off-tumor sample communities. We also performed targeted and untargeted metabolomics, and used the former to quantitatively evaluate our model predictions. A deeper look at the models identified several unexpected but feasible reactions, microbes, and microbial interactions involved in hydrogen sulfide production for which our 16S and metabolomic data could not account. These results will guide future in vitro, in vivo, and in silico tests to establish why hydrogen sulfide production is increased in tumor tissue.

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“…Duran-Pinedo and Frias-Lopez discuss current paradigms of the functional role of the oral microbiome and its components in dysbiosis of oral microbial ecology and its consequence for oral and non-oral diseases [4]. Aruni et al provide recent information and views regarding the newly recognized, fastidious oral pathogen, Filifactor alocis , and the multiple mechanisms used by the microorganism to survive in human oral tissues [5]. Finally, Jakubovics and Burgess describe the critical role played by extracellular DNA in the structure and function of biofilms of the oral cavity [6].…”

mentioning

confidence: 99%