User:S4353567: Difference between revisions
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==Pathology== | ==Pathology== | ||
P. gingivalis is a major pathogen in periodontitis and is part of sublingual plaque | |||
P. gingivalis is a major pathogen in periodontitis and is part of sublingual plaque. 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. | |||
Virulence factors allow this pathogen to become opportunistic. The virulence factors elicit deleterious effects on the host. Virulence factors that are present within P. gingivalis are lipopolysaccharide (LPS), capsular polysaccharide (CPS), fimbriae and gingipains. | |||
LPS is recognised by the Toll like receptors (TLRs), is a stimulator of proinflammatory responses and it also stimulates inflammatory cytokine production such as interleukins and tumour necrosis factors (TNF). Lipid A of P.gingivalis activates TLR2 which dampens the immune response allowing for survival. The CPS or K-antigen is considered to be the capsule of the P.gingivalis and it is able to generate IgG antibody responses. The encapsulated P. gingivalis stains are highly invasive which cause the spread of infection. The fimbriae are filamentious cell surface protrusions that allow for adherence to different types of structures on host cells. Fimbriae also allows for attachment to early colonising bacteria a facilitate in the development of biofilm structure. Gingipains has multiple effects such as deregulating immune responses by stimulting IL-6 etc., confering resistance to P. gingivalis bacterial activity. They also affect vascular permeability and bleeding at the periodontal site. P. gingivalis also inhibits IL-8 accumulation and this had drastic innate immune defense in the periodontium. This results in the decreased capacity of directing leukocytes for the removal of bacteria that are present at these sites, resulting in bacterial overgrowth. | |||
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== | ==Application to biotechnology== | ||
Revision as of 06:53, 22 September 2016
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. It is important to note that although this is a oral microbe P. gingivalis human isolates are both phenotypically and genetically distinct from those recovered from other mammals.
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, obligate anaerobe 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 in its metabolites.
P.gingivalis forms complex biofilms. It is unable to colonise clean tooth surfaces. However it will colonise inflammation site as well as sites that contain gram-positive dental plaque bacteria such as Streptococcus gordonii, which is a primary coloniser on teeth. This provides an attachment site as well as supplying growth substrates.
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 gingival tissue. It is established in the periodontal pocket.
It is able to invade cells, such as epithelial cells, and tissues which allows them to replicate and survive. Invasion is allowed to happen with the aid of major fimbriae which binds to the β1 integrin on the host cell which causes the rearrangement of the actin cytoskeleton to allow internalisations. However when they do invade they do know that they do not initiate apoptosis or necrosis. To allow survival they secrete ATP-hydrolysing enzyme which suppresses ATP-dependent apoptosis. It is also able to spread through cells via actin cytoskeleton bridges. This allows spread without causing host cell death as well as avoiding immune surveillance. Once inside it affects cell-cycle pathways accelerating proliferation of gingival epithelia cells.
Pathology
P. gingivalis is a major pathogen in periodontitis and is part of sublingual plaque. 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.
Virulence factors allow this pathogen to become opportunistic. The virulence factors elicit deleterious effects on the host. Virulence factors that are present within P. gingivalis are lipopolysaccharide (LPS), capsular polysaccharide (CPS), fimbriae and gingipains.
LPS is recognised by the Toll like receptors (TLRs), is a stimulator of proinflammatory responses and it also stimulates inflammatory cytokine production such as interleukins and tumour necrosis factors (TNF). Lipid A of P.gingivalis activates TLR2 which dampens the immune response allowing for survival. The CPS or K-antigen is considered to be the capsule of the P.gingivalis and it is able to generate IgG antibody responses. The encapsulated P. gingivalis stains are highly invasive which cause the spread of infection. The fimbriae are filamentious cell surface protrusions that allow for adherence to different types of structures on host cells. Fimbriae also allows for attachment to early colonising bacteria a facilitate in the development of biofilm structure. Gingipains has multiple effects such as deregulating immune responses by stimulting IL-6 etc., confering resistance to P. gingivalis bacterial activity. They also affect vascular permeability and bleeding at the periodontal site. P. gingivalis also inhibits IL-8 accumulation and this had drastic innate immune defense in the periodontium. This results in the decreased capacity of directing leukocytes for the removal of bacteria that are present at these sites, resulting in bacterial overgrowth.
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
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]
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.]
- ↑ MICR3004
This page is written by Kiranjot Kaur for the MICR3004 course, Semester 2, 2016
