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Nature Communications May 2023Streptococcus mutans has been implicated as the primary pathogen in childhood caries (tooth decay). While the role of polymicrobial communities is appreciated, it...
Streptococcus mutans has been implicated as the primary pathogen in childhood caries (tooth decay). While the role of polymicrobial communities is appreciated, it remains unclear whether other microorganisms are active contributors or interact with pathogens. Here, we integrate multi-omics of supragingival biofilm (dental plaque) from 416 preschool-age children (208 males and 208 females) in a discovery-validation pipeline to identify disease-relevant inter-species interactions. Sixteen taxa associate with childhood caries in metagenomics-metatranscriptomics analyses. Using multiscale/computational imaging and virulence assays, we examine biofilm formation dynamics, spatial arrangement, and metabolic activity of Selenomonas sputigena, Prevotella salivae and Leptotrichia wadei, either individually or with S. mutans. We show that S. sputigena, a flagellated anaerobe with previously unknown role in supragingival biofilm, becomes trapped in streptococcal exoglucans, loses motility but actively proliferates to build a honeycomb-like multicellular-superstructure encapsulating S. mutans, enhancing acidogenesis. Rodent model experiments reveal an unrecognized ability of S. sputigena to colonize supragingival tooth surfaces. While incapable of causing caries on its own, when co-infected with S. mutans, S. sputigena causes extensive tooth enamel lesions and exacerbates disease severity in vivo. In summary, we discover a pathobiont cooperating with a known pathogen to build a unique spatial structure and heighten biofilm virulence in a prevalent human disease.
Topics: Male; Child; Female; Humans; Child, Preschool; Virulence; Dental Caries Susceptibility; Streptococcus mutans; Biofilms
PubMed: 37217495
DOI: 10.1038/s41467-023-38346-3 -
Journal of Indian Society of... 2016With the advent of DNA-based culture-independent techniques, a constantly growing number of Selenomonas phylotypes have been detected in patients with destructive...
BACKGROUND
With the advent of DNA-based culture-independent techniques, a constantly growing number of Selenomonas phylotypes have been detected in patients with destructive periodontal diseases. However, the prevalence levels that have been determined in different studies vary considerably.
AIM
The present study was undertaken to detect and compare the presence of Selenomonas sputigena in the subgingival plaque samples from generalized aggressive periodontitis (GAP), chronic generalized periodontitis, and periodontally healthy patients using conventional polymerase chain reaction (PCR) technique.
MATERIALS AND METHODS
A total of 90 patients were categorized as periodontally healthy individuals (Group I, n = 30), chronic generalized periodontitis (Group II, n = 30), and GAP (Group III, n = 30). The clinical parameters were recorded and subgingival plaque samples were collected. These were then subjected to conventional PCR analysis.
STATISTICAL ANALYSIS USED
Kruskal-Wallis ANOVA test was used for multiple group comparisons followed by Mann-Whitney U-test for pairwise comparison.
RESULTS
On comparison between three groups, all the clinical parameters were found to be statistically highly significant. Comparing Groups I-II and I-III, the difference in detection was found to be statistically highly significant whereas in Groups II-III, it was statistically nonsignificant. On comparison of S. sputigena detected and undetected patients to clinical parameters in various study groups, the difference was found to be nonsignificant.
CONCLUSION
S. sputigena was found to be significantly associated with chronic and aggressive periodontitis. Although the difference in its detection frequency in both groups was statistically nonsignificant when compared clinically, S. sputigena was more closely associated with the GAP.
PubMed: 27563202
DOI: 10.4103/0972-124X.181247 -
Infection and Immunity Feb 2023Increased prevalence and abundance of Selenomonas sputigena have been associated with periodontitis, a chronic inflammatory disease of tooth-supporting tissues, for more...
Increased prevalence and abundance of Selenomonas sputigena have been associated with periodontitis, a chronic inflammatory disease of tooth-supporting tissues, for more than 50 years. Over the past decade, molecular surveys of periodontal disease using 16S and shotgun metagenomic sequencing approaches have confirmed the disease association of classically recognized periodontal pathogens such as Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia while highlighting previously underappreciated organisms such as Filifactor alocis and S. sputigena. Despite abundant clinical association between and periodontal disease, we have little to no understanding of its pathogenic potential, and virulence mechanisms have not been studied. In this study, we sought to characterize the response of gingival epithelial cells to infection with . Here, we show that attaches to gingival keratinocytes and induces expression and secretion of cytokines and chemokines associated with inflammation and leukocyte recruitment. We demonstrate that induces signaling through Toll-like receptor 2 (TLR2) and TLR4 but evades activation of TLR5. Cytokines released from -infected keratinocytes induced monocyte and neutrophil chemotaxis. These results show that S. -host interactions have the potential to contribute to bacterially driven inflammation and tissue destruction, the hallmark of periodontitis. Characterization of previously unstudied pathogens may provide novel approaches to develop therapeutics to treat or prevent periodontal disease.
Topics: Humans; Inflammation; Periodontitis; Porphyromonas gingivalis; Periodontal Diseases; Cytokines; Epithelial Cells
PubMed: 36648232
DOI: 10.1128/iai.00319-22 -
Journal of Pharmacy & Bioallied Sciences 2017Periodontitis is a polymicrobial disease caused by complex interactions between distinct pathogens in a biofilm resulting in the destruction of periodontal tissues. It... (Review)
Review
Periodontitis is a polymicrobial disease caused by complex interactions between distinct pathogens in a biofilm resulting in the destruction of periodontal tissues. It seems evident that unknown microorganisms might be involved in onset or progression of periodontitis. For many decades, research in the field of oral microbiology failed to identify certain subgingival microbiota due to technical limitations but, over a period of 12 years using molecular approaches and sequencing techniques, it became feasible to reveal the existence of new periodontal pathogens. Therefore, it is evident that in addition to conventional periodontal pathogens, other microbes might be involved in onset and progression of periodontitis. The novel pathogens enlisted under periodontal phylogeny include , , , , , , , , and . The polymicrobial etiology of periodontitis has been elucidated by comprehensive techniques, and studies throwing light on the possible virulence mechanisms possessed by these novel periodontal pathogens are enlisted.
PubMed: 28979069
DOI: 10.4103/jpbs.JPBS_288_16 -
Molecular & Cellular Proteomics : MCP Apr 2018Flagellated, Gram-negative, anaerobic, crescent-shaped species are colonizers of the digestive system, where they act at the interface between health and disease. is...
Flagellin Glycoproteomics of the Periodontitis Associated Pathogen Reveals Previously Not Described -glycans and Rhamnose Fragment Rearrangement Occurring on the Glycopeptides.
Flagellated, Gram-negative, anaerobic, crescent-shaped species are colonizers of the digestive system, where they act at the interface between health and disease. is also considered a potential human periodontal pathogen, but information on its virulence factors and underlying pathogenicity mechanisms is scarce. Here we provide the first report of a glycoprotein, showing that produces a diversely and heavily -glycosylated flagellin C9LY14 as a major cellular protein, which carries various hitherto undescribed rhamnose- and -acetylglucosamine linked -glycans in the range from mono- to hexasaccharides. A comprehensive glycomic and glycoproteomic assessment revealed extensive glycan macro- and microheterogeneity identified from 22 unique glycopeptide species. From the multiple sites of glycosylation, five were unambiguously identified on the 437-amino acid C9LY14 protein (Thr149, Ser182, Thr199, Thr259, and Ser334), the only flagellin protein identified. The -glycans additionally showed modifications by methylation and putative acetylation. Some -glycans carried hitherto undescribed residues/modifications as determined by their respective values, reflecting the high diversity of native flagellin. We also found that monosaccharide rearrangement occurred during collision-induced dissociation (CID) of protonated glycopeptide ions. This effect resulted in pseudo Y1-glycopeptide fragment ions that indicated the presence of additional glycosylation sites on a single glycopeptide. CID oxonium ions and electron transfer dissociation, however, confirmed that just a single site was glycosylated, showing that glycan-to-peptide rearrangement can occur on glycopeptides and that this effect is influenced by the molecular nature of the glycan moiety. This effect was most pronounced with disaccharides. This study is the first report on -linked flagellin glycosylation in a species, revealing that C9LY14 is one of the most heavily glycosylated flagellins described to date. This study contributes to our understanding of the largely under-investigated surface properties of oral bacteria. The data have been deposited to the ProteomeXchange with identifier PXD005859.
Topics: Escherichia coli; Flagellin; Glycopeptides; Glycosylation; Periodontitis; Polysaccharides; Proteomics; Recombinant Proteins; Rhamnose; Selenomonas
PubMed: 29339411
DOI: 10.1074/mcp.RA117.000394 -
Clinical Nutrition (Edinburgh, Scotland) Mar 2022Malnutrition has been confirmed to play an important role in colorectal cancer (CRC) progression via the gut microenvironment. However, the characteristics of the gut...
BACKGROUD
Malnutrition has been confirmed to play an important role in colorectal cancer (CRC) progression via the gut microenvironment. However, the characteristics of the gut microbiota or its potential biological mechanism in CRC remain inconclusive.
METHODS
In this work, Patient-Generated Subjective Global Assessment (PG-SGA) tool and 16sRNA sequencing were prepared to detect the variation in gut microbiota and the association between nutrition status and gut microbiota. RDA/CCA analysis was used to evaluate the relationship between faecal microbiota from malnourished CRC and clinical nutrition indicators. To investigate the mechanism of the gut microbiota in CRC, faecal samples from malnourished CRC patients were transplanted into C57BL/6J and DSS/AOM mouse models. Moreover, FACS and IHC were prepared to detect the infiltration of B cells and macrophages. qPCR and Elisa assays were performed to explore the expression of cytokines.
RESULT
We found dramatic variation in the faecal microbiota among patients with different nutritional statuses, discovering that specific microbiota species, namely, Atopobium vaginae, Selenomonas sputigena and Faecalibacterium prausnitzii, may be considered diagnostic biomarkers in malnutrition and indicate poor prognosis. High expression level of A. vaginae in CRC tissues revealed the poorer overall survival compared with low expression level (Mean survival: 23.0 months vs 29.0 months). Faecal from malnourished colorectal cancer were found to be protumorigenic. More importantly, our evidence suggests that after faecal microbiota transplantation, B cells and macrophages are recruited to activate specific tumour immunity in CRC. Depletion of B cells significantly suppressed faecal microbiota-induced M2b polarization as well as the protumorigenic activity of tumour-associated macrophages in vivo.
CONCLUSION
Faecal microbiota in CRC under malnutrition conditions exhibits specific characteristics that accelerate CRC progression and regulate B cells and macrophages. The use of specific faecal microbial species could be a feasible approach for identifying the malnutrition status of patients and demonstrating the poor prognosis of CRC.
Topics: Animals; Colorectal Neoplasms; Feces; Gastrointestinal Microbiome; Humans; Malnutrition; Mice; Mice, Inbred C57BL; Tumor Microenvironment
PubMed: 35124471
DOI: 10.1016/j.clnu.2022.01.001 -
Infection and Immunity Oct 1989Twenty-eight strains of Fusobacterium nucleatum and 41 Selenomonas strains, including S. sputigena (24 strains), S. flueggei (10 strains), S. infelix (5 strains), and S....
Coaggregation of Fusobacterium nucleatum, Selenomonas flueggei, Selenomonas infelix, Selenomonas noxia, and Selenomonas sputigena with strains from 11 genera of oral bacteria.
Twenty-eight strains of Fusobacterium nucleatum and 41 Selenomonas strains, including S. sputigena (24 strains), S. flueggei (10 strains), S. infelix (5 strains), and S. noxia (2 strains), were tested for their ability to coaggregate with each other and with 49 other strains of oral bacteria representing Actinobacillus, Actinomyces, Bacteroides, Capnocytophaga, Gemella, Peptostreptococcus, Porphyromonas, Propionibacterium, Rothia, Streptococcus, and Veillonella species. Selenomonads coaggregated with fusobacteria and with Actinomyces naeslundii PK984 but not with any of the other bacteria, including other selenomonads. In contrast, fusobacteria coaggregated with members of all genera, although not with all strains of each species tested. Each fusobacterium strain appeared to have its own set of partners and coaggregation properties, unlike their partners, whose coaggregation properties in earlier surveys delineated distinct coaggregation groups. Coaggregations of fusobacteria with the 63 gram-negative strains were usually inhibited by EDTA, whereas those with the 27 gram-positive strains were usually not inhibited. Likewise, lactose-inhibitable coaggregations were common among some strains of fusobacteria and some strains from each of the genera containing gram-negative partners but were rarely observed with gram-positive partners. Heating the fusobacteria at 85 degrees C for 30 min completely prevented coaggregation with most partners, suggesting the involvement of a protein on the fusobacteria. Heat treatment of many of the gram-negative partners not only enhanced their coaggregation with the fusobacteria but also changed lactose-sensitive coaggregations to lactose-insensitive coaggregations. Although fusobacteria coaggregated with a broader variety of oral partner strains than any other group of oral bacteria tested to date, each fusobacterium exhibited coaggregation with only a certain set of partner strains, and none of the fusobacteria adhered to other strains of fusobacteria, indicating that recognition of partner cell surfaces is selective. The strains of F. nucleatum are heterogeneous and cannot be clustered into distinct coaggregation groups. Collectively, these results indicate that coaggregation between fusobacteria and many gram-negative partners is significantly different from their coaggregation with gram-positive partners. The contrasting variety of partners for fusobacteria and selenomonads supports the concept of coaggregation partner specificity that has been observed with every genus of oral bacteria so far examined.
Topics: Actinomyces; Bacterial Adhesion; Fusobacterium; Hot Temperature; Lactose; Mouth; Streptococcus; Veillonella
PubMed: 2777378
DOI: 10.1128/iai.57.10.3194-3203.1989 -
Microorganisms May 2020Oral bacteria possess the ability to form biofilms on solid surfaces. After the penetration of oral bacteria into the pulp, the contact between biofilms and pulp tissue...
Oral bacteria possess the ability to form biofilms on solid surfaces. After the penetration of oral bacteria into the pulp, the contact between biofilms and pulp tissue may result in pulpitis, pulp necrosis and/or periapical lesion. Depending on the environmental conditions and the availability of nutrients in the pulp chamber and root canals, mainly Gram-negative anaerobic microorganisms predominate and form the intracanal endodontic biofilm. The objective of the present study was to investigate the role of different substrates on biofilm formation as well as the separate and collective incorporation of six endodontic pathogens, namely and into a nine-species "basic biofilm". This biofilm was formed in vitro as a standard subgingival biofilm, comprising and The resulting endodontic-like biofilms were grown 64 h under the same conditions on hydroxyapatite and dentin discs. After harvesting the endodontic-like biofilms, the bacterial growth was determined using quantitative real-time PCR, were labeled using fluorescence in situ hybridization (FISH) and analyzed by confocal laser scanning microscopy (CLSM). The addition of six endodontic pathogens to the "basic biofilm" induced a decrease in the cell number of the "basic" species. Interestingly, counts increased in biofilms containing and respectively, both on hydroxyapatite and on dentin discs, whereas counts increased only on dentin discs by addition of . The growth of on hydroxyapatite discs and of and on dentin discs were significantly higher in the biofilm containing all species than in the "basic biofilm". Contrarily, the counts of , and on hydroxyapatite discs as well as counts of and on dentin discs decreased in the all-species biofilm. Overall, all bacterial species associated with endodontic infections were successfully incorporated into the standard multispecies biofilm model both on hydroxyapatite and dentin discs. Thus, future investigations on endodontic infections can rely on this newly established endodontic-like multispecies biofilm model.
PubMed: 32384777
DOI: 10.3390/microorganisms8050674 -
Journal of Clinical and Diagnostic... Apr 2015Selenomonas species have been associated with chronic periodontitis and have been implicated in converting periodontal health to disease. Scanty literature is available...
BACKGROUND AND AIM
Selenomonas species have been associated with chronic periodontitis and have been implicated in converting periodontal health to disease. Scanty literature is available in Indian population. Hence, the objective of the study was to detect the prevalence of Selenomonas sputigena in healthy and chronic periodontitis by polymerase chain reaction (PCR) in Indian population and to check whether smoking affects the subgingival microflora of this organism in chronic periodontitis.
MATERIALS AND METHODS
A total of 60 subjects with severe chronic periodontitis with or without smoking and periodontal healthy subjects underwent clinical and microbiological assessment. A deep subgingival plaque sample was collected and genomic DNA was extracted from each sample and analysed for detection of Selnomonas sputigena using PCR. The frequency and quantification of bacteria were also estimated.
RESULTS
All groups differed statistically significant in the frequency of detection of Selenomonas sputigena. On comparison of patients with chronic periodontitis in smokers and non-smokers, there was no statistically significant difference. When the results were quantified, statistically non-significant results were seen among all groups. Plaque index, gingival index, probing pocket depth and clinical attachment level were statistically non-significant in chronic periodontitis with smokers and non-smokers.
CONCLUSION
Prevalence of Selenomonas sputigena showed significant differences with respect to the frequency of detection when comparing the disease group to the healthy population. But no significant difference was seen when the results were quantified. Smoking has no influence on number of Selenomonas sputigena. This study highlights presence as well as quantity of the organism is very important in elucidating its role in causation and progression of the disease.
PubMed: 26023635
DOI: 10.7860/JCDR/2015/12550.5782 -
Journal of Dental Research Jun 2016In recent years, several new periodontal taxa have been associated with the etiology of periodontitis. A recent systematic review provides further support for the...
In recent years, several new periodontal taxa have been associated with the etiology of periodontitis. A recent systematic review provides further support for the pathogenic role of 17 species/phylotypes. Thus, the aim of this study was to assess the prevalence and levels of these species in subjects with generalized chronic periodontitis (GChP; n = 30), generalized aggressive periodontitis (GAgP; n = 30), and periodontal health (PH; n = 30). All subjects underwent clinical and microbiological assessment. Nine subgingival plaque samples were collected from each subject and analyzed for their content of 20 bacterial species/phylotypes through the RNA-oligonucleotide quantification technique. Subjects from the GChP and GAgP groups presented the highest mean values for all clinical parameters in comparison with the PH group (P < 0.05). Subjects with GChP and GAgP showed significantly higher mean levels of Bacteroidetes sp. human oral taxon (HOT) 274, Fretibacterium sp. HOT 360, and TM7 sp. HOT 356 phylotypes, as well as higher mean levels of Filifactor alocis, Fretibacterium fastidiosum, Porphyromonas gingivalis, Tannerella forsythia, and Selenomonas sputigena species than PH subjects (P < 0.05). GAgP subjects presented higher mean levels of TM7 sp. HOT 356 and F. alocis than GChP subjects (P < 0.05). A significantly higher mean prevalence of Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, and Fretibacterium sp. HOT 362 was found in subjects with GChP and GAgP than in PH subjects. Mean levels of P. gingivalis (r = 0.68), T. forsythia (r = 0.62), F. alocis (r = 0.51, P = 0.001), and Fretibacterium sp. HOT 360 (r = 0.41) were correlated with pocket depth (P < 0.001). In conclusion, Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, Fretibacterium sp. HOT 362, and TM7 sp. HOT 356 phylotypes, in addition to F. alocis, F. fastidiosum, and S. sputigena, seem to be associated with periodontitis, and their role in periodontal pathogenesis should be further investigated.
Topics: Aggressive Periodontitis; Bacteria; Bacteroides; Bacteroidetes; Biofilms; Chronic Periodontitis; Dental Plaque; Humans; Microbiota
PubMed: 26936213
DOI: 10.1177/0022034516634619