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Porphyromonas gingivalis

Higher order taxa

Bacteria – Bacteria – Bacteroidetes – Bacteroidetes – Bacteroidales – Porphyromonadaceae – Porphyromonas

Species

P. gingivalis W83 Species name and type strain (consult LPSN http://www.bacterio.net/index.html for this information)

Description and significance

Porphyromonas gingivalis is a gram-negative obligate anaerobe that is non-motile and pathogenic. The bacterium is rod-shaped and is found in the oral cavity and has been strongly implicated as a pathogen in periodontitis [1], a damaging disease where the supporting structures of teeth and the gingiva are affected. It can also be found in the upper gastrointestinal tract, the respiratory tract, and the colon. P. gingivalis can be found under conditions of both health and disease, where the prevalences identified to range from 10% to 25% in healthy individuals and 79% to 90% in those with periodontitis [2]. Previous studies in epidemiology have revealed that P. gingivalis strains differ depending on their human disease association [3]. Furthermore, studies using different animal models have also demonstrated that strains of P. gingivalis vary in their virulence, whether it be in soft tissue destruction or death, with some being classified as virulent (e.g. strain W83) and others being identified as being avirulent [4].

The virulent strain W83 has been cultured and can be obtained from the American Type Culture Collection (ATCC). This bacterium was originally isolated from an undocumented human oral infection in Bonn, Germany in the 1950s. P. gingivalis has been recognised as an opportunistic pathogen of the oral mucosa and can be found in oral biofilms. Onset and progression of chronic periodontitis has been associated with this bacterium. This bacterium produces an enzyme, collagenase, that degrades collagen observed in chronic periodontal disease. In addition, P. gingivalis can induce secretion of cytokines from immune cells when they invade into hosts. The cytokines that are released are present in inflamed gingiva and result in aggravation of the oral gingival tissues and alveolar bone leading to damage [5].

The structural components of P. gingivalis include the capsule, outer membrane containing various proteins, lipopolysaccharide (LPS), bacterial fimbriae and proteinases. These structures all have functions in the pathogenesis of periodontitis in individuals. The virulence factors of the pathogenic bacterium P. gingivalis (W83) should be further studied due to the microbes propensity to cause disease by invading gingival epithelial cells and evade host defences and immune responses [6]. In order to effectively control this bacterium in human pathology, more research needs to be conducted in order to find effective control measures against it.

Give a general description of the species (e.g. where/when was it first discovered, where is it commonly found, has it been cultured, functional role, type of bacterium [Gram+/-], morphology, etc.) and explain why it is important to study this microorganism. Examples of citations [1], [2].

Genome structure

The genome of P. gingivalis W83 is circular, 2,343,479bp long, and with an average G+C content of 48.3% [7]. Four ribosomal operons (5S-23S-tRNAAla-tRNAIle-16S), two structural RNA gases and fifty-three tRNA genes with specificity for all 20 amino acids [7]. Furthermore, 1,990 ORFs have been identified in the genome [8]. Of the 1,990 ORFs, 1,075 (54%) were identified to be involved in biological roles, 184 (9.2%) were conserved hypothetical proteins or conserved domain proteins, 208 (10.5%) were of unknown function, and 523 (26.3%) encoded hypothetical proteins [9].

It has also been identified that 6% of the genome are made up of repetitive elements and fall into two classes: DNA repeats and transposable elements [9]. The DNA repeats identified include uninterrupted direct repeats and clustered regularly interspaced short palindromic repeats (CRSPRs). Moreover, transposable elements detected include insertion sequence (IS) elements, miniature inverted-repeat transposable elements (MITEs) and large stretches of genes that of conjugal and mobilisable transposons [9].

Select a strain for which genome information (e.g. size, plasmids, distinct genes, etc.) is available.

Cell structure and metabolism

The bacterium cellular structure is made up of the capsule, fimbriae, LPS and outer membrane containing various proteins. The capsule of P. gingivalis has been identified to play an important role in aiding evasion of host immune system activation, promotes survival of the bacterium within the host cells, and increasing virulence [10]. Studies have determined that the the capsule of W83 decreased the production of leukocytes indicating that the capsular structure and adhesion capacity increase virulence [11]

For the bacterium to get established in the oral cavity, first there must be adhesion to the teeth or mucosal surfaces. Adherence to host surfaces is facilitated by adhesins on the surface of the bacteria, as either cell wall components or associated with other surface structures, interacting with receptors of cells in the mouth[12]. The adhesins found on the capsule functions as method of providing resistance to the flow of saliva.

Studies have identified that P. gingivalis expresses two distinct fimbriae on its cell surface: FimA (long, major fimbriae, role in attachment and biofilms) and Mfa (short, minor or Mfa1 fimbriae, cell-cell adhesion and microcolony formation) [11]. Depending on the strain, the FimA protein varies and has been classified into six types: types I-V and Ib [11. The W83 strain contains type IV FimA that are poorly fimbriated [11].

LPS is a key factor in the causation of periodontitis. In periodontitis lesions, gingival fibroblasts may directly interact with P. gingivalis and its bacterial products, including LPS [12]. Due to LPSs ability to potently activate host inflammatory and innate immune responses by inducing pro inflammatory cytokines leading to periodontal tissue destruction.

The bacterial cell membrane acts as a selective barrier that offers protection and allows movements of substances through outer membrane porin proteins [13]. The few major proteins in the membrane serve as antigens that host immune cells recognise. Furthermore, the formation and maintenance of periodontal biofilms is a result of outer membrane proteins interacting with periodontal microflora [14].

The P. gingivalis strain W83 is capable of glycolysis and gluconeogenesis when in need of energy or glucose. In addition, the bacterium is also capable of performing the TCA cycle and oxidative phosphorylation.


Cell wall, biofilm formation, motility, metabolic functions.

Ecology

Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.

Pathology

Do these microorganisms cause disease in the oral cavity or elsewhere?

Application to biotechnology

Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…

Current research

Summarise some of the most recent discoveries regarding this species.

References

1. Alpagot, T., Wolff, L. F., Smith, Q. T., & Tran, S. D. (1996). Risk indicators for periodontal disease in a racially diverse urban population. Journal of Clinical Periodontology, 23(11), 982-988. doi:10.1111/j.1600-051X.1996.tb00524.x

2. Griffen, A. L., Becker, M. R., Lyons, S. R., Moeschberger, M. L., & Leys, E. J. (1998). Prevalence of Porphyromonas gingivalis and Periodontal Health Status. Journal of Clinical Microbiology, 36(11), 3239-3242.

3. Amano, A., Kuboniwa M Fau - Nakagawa, I., Nakagawa I Fau - Akiyama, S., Akiyama S Fau - Morisaki, I., Morisaki I Fau - Hamada, S., & Hamada, S. Prevalence of specific genotypes of Porphyromonas gingivalis fimA and periodontal health status. (0022-0345 (Print)).

4. Grenier, D., & Mayrand, D. (1987). Selected characteristics of pathogenic and nonpathogenic strains of Bacteroides gingivalis. Journal of Clinical Microbiology, 25(4), 738-740.

5. Baker, P. J. The role of immune responses in bone loss during periodontal disease. (1286-4579 (Print)).

6. Mysak, J., Podzimek, S., Sommerova, P., Lyuya-Mi, Y., Bartova, J., Janatova, T., . . . Duskova, J. (2014). Porphyromonas gingivalis: Major Periodontopathic Pathogen Overview. Journal of Immunology Research, 2014, 8. doi:10.1155/2014/476068

7. Nelson, K. E., Fleischmann, R. D., DeBoy, R. T., Paulsen, I. T., Fouts, D. E., Eisen, J. A., . . . Fraser, C. M. (2003). Complete Genome Sequence of the Oral Pathogenic Bacterium Porphyromonas gingivalis Strain W83. Journal of Bacteriology, 185(18), 5591-5601. doi:10.1128/JB.185.18.5591-5601.2003

8. Delcher, A. L., Harmon D Fau - Kasif, S., Kasif S Fau - White, O., White O Fau - Salzberg, S. L., & Salzberg, S. L. Improved microbial gene identification with GLIMMER. (0305-1048 (Print)). doi:D - NLM: PMC148753 EDAT- 1999/11/11 MHDA- 1999/11/11 00:01 CRDT- 1999/11/11 00:00 AID - gkc675 [pii PST - ppublish]

9. Riley, M. Functions of the gene products of Escherichia coli. (0146-0749 (Print)). doi:D - NLM: PMC372942 EDAT- 1993/12/01 MHDA- 1993/12/01 00:01 CRDT- 1993/12/01 00:00 PST - ppublish

10. Singh, A., Wyant, T., Anaya-Bergman, C., Aduse-Opoku, J., Brunner, J., Laine, M. L., . . . Lewis, J. P. (2011). The Capsule of Porphyromonas gingivalis Leads to a Reduction in the Host Inflammatory Response, Evasion of Phagocytosis, and Increase in Virulence. Infection and Immunity, 79(11), 4533-4542. doi:10.1128/IAI.05016-11

11. How, K. Y., Song, K. P., & Chan, K. G. (2016). Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Frontiers in Microbiology, 7, 53. doi:10.3389/fmicb.2016.00053

12. Marcotte H & Lavoie MC. (1998). Oral microbial ecology and the role of salivary immunoglobulin A. Microbiology and molecular biology reviews, 62(1), 71-109

13. Nikaido, H. (2003). Molecular Basis of Bacterial Outer Membrane Permeability Revisited. Microbiology and molecular biology reviews, 67(4), 593-656. doi:10.1128/MMBR.67.4.593-656.2003

14. Bos, M. P., Robert, V., & Tommassen, J. (2007). Biogenesis of the Gram-Negative Bacterial Outer Membrane. Annual Review of Microbiology, 61(1), 191-214. doi:10.1146/annurev.micro.61.080706.093245

  1. MICR3004

This page is written by Richard Leung for the MICR3004 course, Semester 2, 2016