Selenonomas noxia
MICR3004 Microbial Genomics Semester 2 2016, The University of Queensland
Corynebacterium matruchotii
Porphyromonas gingivalis
Porphyromonas endodontalis
Kingella oralis
Capnocytophaga gingivalis
Veillonella parvula
Rothia dentocariosa
Classification
Higher order taxa
Bacteria – Terrabacteria group - Firmicutes – Negativicutes – Selenomonadales – Selenomonadaceae – Selenomonas [1]
Species
Species: “Selenomonas noxia” Type strain: ATCC 43541=JCM 8546=VPI D9B-5 [2]
Description and significance
“Selenomonas noxia” (“S. noxia”) is one of five “Selenomonas” species that Moore et al. first characterised in 1987 [3]. “S. noxia” fits the general Selenomonad description- motile, crescent-shaped, nonsporeforming gram-negative rods [3] [4] [5] [6]. It is morphologically distinguishable from other “Selenomonas” species by its relatively smaller cells (1.1 um diameter by 1.1–3.2 um length) [3]. It was first characterised from cultured isolates of the gingival crevice of periodontitis and gingivitis patients. “S. noxia” grow in anaerobic culture, showing abundant growth on peptone-yeast extract media with glucose, mannose, sorbitol, or sorbose [3]. “S. noxia” have one or more central-to-pole flagella originating from the concave cell side [3] [6].
In a healthy oral microbiome, “S. noxia” occurrence strongly correlates with numerous other species: “Actinomyces gerencseriae”, “A. oris”, “A. johnsonii”, “S. sputigena”, “S. artemides”, “Streptococcus sanguinis”, “S. oralis”, “Fusobacterium nucleatum” and “Veillonella parvula”. These bacteria appear to contribute similar functions, with 98% overlap in encoded functions from a 60% overlap in genes. In the functional specialization present, “S. noxia” is one of six rare taxa within the oral microbiome that contribute genes for motility and chemotaxis [7].
“S. noxia” is important to study due to its consistent association with periodontal disease. It is thought to be a putative periodontal pathogen [4] [6] [8] [9]. Periodontitis is a highly prevalent diseasese, and much remains unclear about the mechanisms of its pathogenesis [7]. Elucidation of the exact role “S. noxia” plays in periodontitis initiation and progression, and the mechanism by this occurs, could inform new disease prevention and treatment methods.
Genome structure
The “S. noxia” type strain ATCC 4351 genome has been characterised by whole genome shotgun sequencing. With a size of 2.05499 Mb and GC content of 55.80%, the genome contains 1,983 distinct genes encoding for 1,876 proteins. No plasmids have been detected [10].
Cell structure and metabolism
Cell wall
Negativicutes class members, including “S. noxia”, are distinct from other firmicutes in staining Gram-negative. They have typical gram-negative envelope composition: inner phospholipid leaflet, periplasmic space with a thin peptidoglycan layer, outer lipopolysaccharide leaflet. Significant amounts of the polyamine putrescine have been detected in “S. noxia” peptidoglycan [11].
Motility
“S. noxia” achieve tumbling motility via a flagella tuft attached to the cell curvature [3] [6].
Biofilm formation
“S. noxia” are part dental plaque, a structurally and functionally organized biofilm. Teles et al. found that S. noxia are one of the last species to colonise, increasing significantly in mean proportion after seven days without oral hygiene [12].
Metabolic functions
“S. noxia” are saccharolytic obligate anaerobes, meaning they metabolise sugars to produce energy without oxygen [8]. “S. noxia” typically ferment glucose and fructose to produce acetic and lactic acids, and major amounts of propionic acid [3] [6] [8]. They are distinct from other known “Selenomonas” species by an inability to ferment sucrose [3]. Moore et al. found that 27% of strains can respire via oxidative phosphorylation [3]. These strains have a partial electron transport chain of complexes I and II, and a bd terminal reductase. Nitrate is the terminal electron acceptor [13].
“S. noxia” are hydrogen-forming bacteria, with hydrogen detected in culture [3]. H2 production occurs in anaerobes as a means to reoxidize NADH, which can become overly reduced in fermenters. “S. noxia” encode for several hydrogen production pathways [14].
Ecology
“S. noxia” are strict anaerobes, located in the gingival crevice, and subgingival plaque adjacent to periodontal lesions [3]. They can act as both commensals and pathogens.
“S. noxia” appear to interact relatively little with other oral bacterial species. Five major bacterial complexes are consistently detected in subgingival plaque. “S. noxia” are an outlier, participating in no complexes [15] [16]. Isolates aggregate with the narrowest range of partners observed to date compared with Actinomyces, Bacteroides, Capnocytophaga, Haemophilus, Streptococcus and Veillonella species. Importantly, “S. noxia” do aggregate with Fusobacteria [16]. “Fusobacterium nucleatum” provides a physical tether for late colonisers and oral pathogens such as “S. noxia” to adhere to dental plaque [17].
Pathology
Periodontitis
Hundreds of microbes have insofar been identified within the gingival crevice and periodontal pocket. While little literature exists on “S. noxia” pathogenicity, it is one of the few species that appear to contribute significantly to periodontitis establishment and progression [4].
Periodontitis is a highly prevalent infectious disease. Tooth-supporting tissues become inflamed and periodontal pockets form, with the ultimate result of alveolar bone and periodontal attachment loss [18]. Disease develops with a shift in the subgingival microbiome away from a health-compatible state [7]. A trend toward anaerobes is typical [19]. Disease progresses via complex interactions between dental biofilms and the host’s immune system [18].
Moore et al.’s early studies suggested “S. noxia” were associated with periodontitis. The epithet ‘noxia’ refers to their harmful nature. Data revealed “S. noxia” increased from 0.9% to 5.9% in periodontal plaque from healthy to disease-active sites [3]. Many studies have since confirmed this finding [9] [19] [20] [21] [22]. Data cannot yet conclusively relate “S. noxia” to periodontitis etiology. Nonetheless, considerable literature supports this hypothesis [4] [5] [6] [9] [21]. Tanner et al. found that active-disease patients were distinguished by higher “S. noxia” mean proportions [21]. Association studies demonstrated no combination of species shows a stronger relationship with recent attachment loss than that of “S. noxia” by itself [20]. This suggests “S. noxia” may be involved with general aggressive periodontitis (GAP), a more destructive disease form. Supporting this, “S. noxia” have been detected in GAP lesions [4] and research shows “Selenomonas” phylotypes are typical and abundant members of GAP subgingival biofilm that contribute to structural organisation [22].
Gingival tissue is highly susceptible to lipopolysaccharide (LPS) endotoxins [6]. Among other bacterial products, LPS can trigger host inflammatory cascades. It stimulates cytokine production, which promotes destructive metalloproteinase matrix release of from host tissues [18]. “S. noxia” LPS possesses endotoxic properties stronger than that of “Escherichia coli” LPS [6], suggesting “S. noxia” LPS contributes to periodontal disease progression.
Halitosis
“S. noxia” have been implicated in halitosis. They produce volatile sulphur compounds, responsible for the bad breath associated with halitosis [23].
Obesity
Research suggests “S. noxia” may be involved obesity development. “S. noxia” at levels >1.05% of the total bacterial population can predict obesity with a sensitivity of 98% and specificity of 80% [5]. More research is needed to elucidate the exact relationship between oral bacteria and obesity.
Application to biotechnology
Biotechnologically relevant compound production
“S. noxia” produce propionate via fermentation [3]. Propionate and its derivatives are Food and Drug Administration approved “Generally Recognised As Safe” food additives. They are widely used as antimicrobial and anti-inflammatory agents, herbicides, food preservatives and artificial flavours [24]. Propionate mass production currently occurs largely by chemical synthesis. Interest in microbial production techniques is however growing in response to the environmental issues of conventional synthesis [24]. “S. noxia” could thus play a role in future propionate production.
“S. noxia” are hydrogen-forming bacteria [3]. Hydrogen is a biogas, which could provide a viable, clean alternative to fossil fuels. It has a high calorific value, is efficient, and can be used in fuel cells [25].
==Current research==
Smoking and the oral microbiome
Smoking negatively affects the subgingival microbiome in both periodontal health and disease by supporting pathogen-rich community formation. Interestingly, Tsigarida et al. recently identified that “S. noxia” is a part of the non-smoker core microbiome. Relative abundance was significantly higher in healthy non-smokers than healthy smokers [36].
Cyclic dinucleotides
Bacteria can sense and respond to their environment via secondary messenger molecules. Cyclic dinucleotides appear to be significant biofilm establishment and growth regulators. “S. noxia” produce detectable levels of cyclic dinucleotides [27]. Cyclic dinucleotide regulation interference could present an effective approach to fighting infectious diseases, including periodontitis sustained by “S. noxia”.
References
1. [1]
2. [2]
10. [3]
11. [https://www.jstage.jst.go.jp/article/jgam/48/3/48_3_177/_article Hamana, K., Saito, T., Okada, M., Sakamoto, A., and Hosoya, R. (2002). Covalently linked polyamines in the cell wall peptidoglycan of “Selenomonas”, “Anaeromusa”, “Dendrosporobacter”, “Acidaminococcus” and “Anaerovibrio” belonging to the “Sporomusa” subbranch. J Gen Appl Microbiol, 48: 177-80.]
13. [4]
14. [5]
27. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5478684/ Gürsoy, U. K., Gürsoy, M., Könönen, E., and Sintim, H. O. (2017). Cyclic Dinucleotides in Oral Bacteria and in Oral Biofilms. Front Cell Infect Microbiol 7: 273.}
This page is written by Margot Bligh for the MICR3004 course, Semester 2, 2017
