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Kiranjot Kaur Bench C 43535675 [1]

Porphyromonas gingivalis

Classification

Higher order taxa

Bacteria (Kindom) – Bacteria (Domain) – Bacteroidetes (Phylum) – Bacteroidia (Class) – Bacteroidales (Order) – Prophyeomonadaceae (Family) – Prophyromonas (Genus)

Species

P. gingivalis Type Strain ATCC 33277 [1]

Description and significance

Porphyromonas gingivalis, previously named Bacteriodes gongivalis, is a gram negative bacterium which occurs as coccobacilli or as long rods (0.5 by 1.0 to 2.0 microm). This organism is a major pathogen in chronic periodontitis. Although it is a natural member of the human oral microbiome it can become highly destructive and proliferate rapidly and is able to destroy periodontal tissues causing disease. However, P. gingivalis is detected in very low numbers in healthy individuals. It is a secondary colonizer of dental plaque.

It was first isolated by Slots from a human gingival sulcus. P. gingivalis has an absolute requirement for iron for its growth and is able to be cultured on blood agar with hemin and menadione. It forms small 1 to 2mm convex colonies with brown to black pigment. P. gingivalis is a fermentative organism.

Genome structure

Using the type strain P. gingivalis has a circular genome with no plasmids found. It contains 2,354,866 nucleotides with 2154 genes and of those 2089 are protein encoding genes and 65 RNA encoding genes. This strain contains no pseudogenes and the DNA base composition is 46.5 to 48.4 mol% of G+C. The 16S rRNA sequence for this strain is X73964.

Cell structure and metabolism

P. gingivalis, being a gram negative bacterium it contains a cell wall with peptidoglycan with lysine as the diamino acid. This bacteria contains fimbriae involved in cell invasion along with hemaglutinins and proterinases.

P. gingivalis is a non-motile organism and utilises iron and protoporphyrin IX for its growth. Protoporphyrin IX is a carrier for divalent cations and is an essential prosthetic group for heme. It can be cultured in the presence of heme and its growth is markedly affected by the presence of protein hydrolysates. P. gingivalis contains five major hemagglutinin genes (hagA, hagB, hagC, hagD and hagE) allowing for absorption, invasion of the bacteria in to cells as well as iron utilisation.

P. gingivalis utilises several amino acids for its growth such as aspartate, arginine, cystine, histidine, serine, tryptophan, etc. It has fermentation products such as n-butyric, isobutyric, propionic, iso-valeric and acetic acids. They are also able to produce low levels of other acids such as phenylacetic acids. Proteases like collagenase are detected.

Ecology

P. gingivalis is an obligate anaerobic bacterium that resides in the oral cavity. It is a natural member of the oral microbiome and is a late coloniser. It is found in close proximity to and interacts with juxtaposing gingical tissue. This organism is able to avoid immune surveillance and is able to invade cells and tissue to allow for its replication and growth. It is established in the periodontal pocket.

Pathology

P. gingivalis is a major pathogen in periodontitis and is part of sublingual plaque. It invades macrophages to limit exposure to the extracellular environment and is also able to evade the immune system. The strain differences in P. gingivalis can influence virulence. This pathogen has also been linked in with systemic diseases such as cardiovascular diseases. It is able to invade epithelial, endothelial and smooth muscular cells. It can be aided in entering in to the circulation of the body via eating. P. gingivalis is able to invade cardiovascular cells invasion of cells allows access to host proteins and iron, which are essential for its survival. It has been found to be present in artheromas of the circulatory system. Invasion allows persistence of the pathogen in infected tissue allowing to avoid humoral and cellular responses. Intracellular survival also provides protection against antibiotics.

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. LPSN: List of Prokaryotic names with Standing in Nomenclature

2. Human Oral Microbiome

3. Olczak, T., Simpson, W., Liu, X., & Genco, C. A. (2005). Iron and heme utilization in Porphyromonas gingivalis. FEMS microbiology reviews, 29(1), 119-144.

4. [https://hindawi.com/journals/jir/2014/476068/ Mysak, J., Podzimek, S., Sommerova, P., Lyuya-Mi, Y., Bartova, J., Janatova, T., Prochazkova, J. and Duskova, J. (2014). Porphyromonas gingivalis: major periodontopathic pathogen overview. Journal of immunology research, 2014. Chicago]

5. Pandit Pandit, N., Changela, R., Bali, D., Tikoo, P., & Gugnani, S. (2015). Porphyromonas gingivalis: Its virulence and vaccine. Journal of the International Clinical Dental Research Organization, 7(1), 51.

4. [Bostanci, N., & Belibasakis, G. N. (2012). Porphyromonas gingivalis: an invasive and evasive opportunistic oral pathogen. FEMS microbiology letters, 333(1), 1-9.]

5. [Olsen, I., & Progulske-Fox, A. (2015). Invasion of Porphyromonas gingivalis strains into vascular cells and tissue. Journal of oral microbiology, 7.]

6. [Kastelein, P., Van Steenbergen, T. J. M., Bras, J. M., & De Graaff, J. (1981). An experimentally induced phlegmonous abscess by a strain of Bacteroides gingivalis in guinea pigs and mice. Antonie Van Leeuwenhoek, 47(1), 1-9.]

7. [Shah, H. N., & Collins, M. D. (1988). Proposal for reclassification of Bacteroides asaccharolyticus, Bacteroides gingivalis, and Bacteroides endodontalis in a new genus, Porphyromonas. International Journal of Systematic and Evolutionary Microbiology, 38(1), 128-131.]

8. [COYKENDALL, A. L., KACZMAREK, F. S., & SLOTS, J. (1980). Genetic Heterogeneity in Bacteroides asaccharolyticus (Holdeman and Moore 1970) Finegold and Barnes 1977 (Approved Lists, 1980) and Proposal of Bacteroides gingivalis sp. nov. and Bacteroides macacae (Slots and Genco) comb. nov. International Journal of Systematic and Evolutionary Microbiology, 30(3), 559-564.]

9. [SLOTS, J. (1977). The predominant cultivable microflora of advanced periodontitis. European Journal of Oral Sciences, 85(2), 114-121.]

10. [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.]

11. [Konig, M. F., Paracha, A. S., Moni, M., Bingham, C. O., & Andrade, F. (2014). Defining the role of Porphyromonas gingivalis peptidylarginine deiminase (PPAD) in rheumatoid arthritis through the study of PPAD biology. Annals of the rheumatic diseases, annrheumdis-2014.]

12. [Kuboniwa, M., Hendrickson, E. L., Xia, Q., Wang, T., Xie, H., Hackett, M., & Lamont, R. J. (2009). Proteomics of Porphyromonas gingivalis within a model oral microbial community. BMC microbiology, 9(1), 1.]

13. [Nelson, K.E., Fleischmann, R.D., DeBoy, R.T., Paulsen, I.T., Fouts, D.E., Eisen, J.A., Daugherty, S.C., Dodson, R.J., Durkin, A.S., Gwinn, M. and Haft, D.H. (2003). Complete genome sequence of the oral pathogenic bacterium Porphyromonas gingivalis strain W83. Journal of bacteriology, 185(18), 5591-5601.]

14. [Yoshimoto, H., Takahashi, Y., Hamada, N., & Umemoto, T. (1993). Genetic transformation of Porphyromonas gingivalis by electroporation. Oral microbiology and immunology, 8(4), 208-212.]

15. Summary of Porphyromonas gingivalis, Strain ATCC 33277

16. [Darveau, R.P., Pham, T.T.T., Lemley, K., Reife, R.A., Bainbridge, B.W., Coats, S.R., Howald, W.N., Way, S.S. and Hajjar, A.M. (2004). Porphyromonas gingivalis lipopolysaccharide contains multiple lipid A species that functionally interact with both toll-like receptors 2 and 4. Infection and immunity, 72(9), 5041-5051.]

17. [Ang, C. S., Veith, P. D., Dashper, S. G., & Reynolds, E. C. (2008). Application of 16O/18O reverse proteolytic labeling to determine the effect of biofilm culture on the cell envelope proteome of Porphyromonas gingivalis W50. Proteomics, 8(8), 1645-1660.]

18. [Curtis, M.A., Opoku, J.A., Rangarajan, M., Gallagher, A., Sterne, J.A.C., Reid, C.R., Evans, H.E.A. and Samuelsson, B. (2002). Attenuation of the virulence of Porphyromonas gingivalis by using a specific synthetic Kgp protease inhibitor. Infection and immunity, 70(12), 6968-6975.]

19. [Olsen, I., & Yilmaz, Ö. (2016). Modulation of inflammasome activity by Porphyromonas gingivalis in periodontitis and associated systemic diseases. Journal of oral microbiology, 8.]

20. [Burmistrz, M., Dudek, B., Staniec, D., Martinez, J. I. R., Bochtler, M., Potempa, J., & Pyrc, K. (2015). Functional analysis of Porphyromonas gingivalis W83 CRISPR-Cas systems. Journal of bacteriology, 197(16), 2631-2641.]

21. [Lam, R. S., O’Brien-Simpson, N. M., Holden, J. A., Lenzo, J. C., Fong, S. B., & Reynolds, E. C. (2016). Unprimed, M1 and M2 Macrophages Differentially Interact with Porphyromonas gingivalis. PloS one, 11(7), e0158629.]

22. [Nakao, R., Hasegawa, H., Dongying, B., Ohnishi, M., & Senpuku, H. (2016). Assessment of outer membrane vesicles of periodontopathic bacterium Porphyromonas gingivalis as possible mucosal immunogen. Vaccine, 34(38), 4626-4634.]

23. [Ho, M. H., Chen, C. H., Goodwin, J. S., Wang, B. Y., & Xie, H. (2015). Functional advantages of Porphyromonas gingivalis vesicles. PloS one, 10(4), e0123448.]

24. [Carvalho-Filho, P. C., Gomes-Filho, I. S., Meyer, R., Olczak, T., Xavier, M. T., & Trindade, S. C. (2016). Role of Porphyromonas gingivalis HmuY in immunopathogenesis of chronic periodontitis. Mediators of Inflammation, 2016.]

25. [Olczak, T., Sosicka, P., & Olczak, M. (2015). HmuY is an important virulence factor for Porphyromonas gingivalis growth in the heme-limited host environment and infection of macrophages. Biochemical and biophysical research communications, 467(4), 748-753.]

  1. MICR3004

This page is written by Kiranjot Kaur for the MICR3004 course, Semester 2, 2016