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==Ecology==
==Ecology==


Aerobe/anaerobe, habitat (location in the oral cavity, potential other environments) and microbe/host interactions.REEEEEEEEEEEEEEEEEEEEEEEEE<ref name="bean" />
P. gingivalis makes up a major component of the human oral microbiome, and has successfully colonised the epithelial cells of the gingiva(6). It is a compulsively anaerobic species, so cannot survive in the presence of oxygen. It can often be found in what is termed a ‘red complex’ in conjunction with Treponema denticola, and Tannerella forsythia. This complex is strongly associated with periodontal disease (7). Despite its well-researched connection with PATHOLOGY, P. gingivalis is found in numbers of patients not displaying clinical pathology (6). In general, bacteria colonising the mouth are tolerant towards and tolerated by the immune system, because inflammation leading to loss of teeth will eventually kill both the host and the bacteria (8). This is why some of the bacteria do not produce a negative reaction in the host. P. gingivalis colonises epithelial cells in the gingival compartment, which sometimes detect the bacteria and release inflammatory cytokines, however no particular apoptosis is noted in colonised cells (6). The bacteria is able to adhere to the epithelial cells due to its fimbriae, and enter the cells by binding to the β1 integrin receptor (6). It is capable of intracellular replication. Infected cells as with colonised cells do not display apoptosis, as the typical apoptotic pathways are inhibited by P. gingivalis while it replicates. In this way the bacteria is able to maintain viability within the epithelial cells for large amounts of time (6). The mouth seems to be the only habitat that this bacteria can survive in, as there is no evidence of free-living P. gingivalis (8). This makes sense, as the bacteria has very restrictive metabolic requirements. It is also suggested that the surface of the tooth may be required for colonisation, which is another factor reducing the ability of P. gingivalis to replicate outside the oral cavity. The evidence supporting this hypothesis is that the bacteria has not been cultured from edentulous babies or elderly (8). Other mammalian species are colonised by P. gingivalis, however the strains are genetically dissimilar and distinct.


==Pathology==
==Pathology==

Revision as of 05:21, 23 September 2016

Thomas Clarkson, Bench D, 31/08/16.


Classification

re re re

Higher order taxa

Bacteria – Bacteria – Bacteroidetes – Bacteroidetes – Bacteroidales – Porphyromonas - gingivalis

Species

The species is Porphyromonas gingivalis, and it has a number of different type strains. These are 2561 T , ATCC 33277 T , BCRC 14417 T , CCRC 14417 T , CCUG 25893 T , CCUG 25928 T , CIP 103683 T , Coykendall 2561T , DSM 20709 T , JCM 12257 T , KCTC 5121T , NCTC 11834 T , Slots 2561 T , Slots' 2561 T , Slots' strain 2561 T (1).

' 'it is a strain[1]

or is it a strain?[1]

Description and significance

Porphyromonas gingivalis, is a gram-negative rod bacteria. It is non-motile, and found on and within the gingival epithelial cells in the oral cavity. It is dark-pigmented, asaccharolytic, and requires iron from heme for growth (2). Its relative importance comes from its implication as the most common cause of periodontitis. A number of articles have demonstrated its role as the aetiological agent. Overall, around 85% of diseased tissues have been shown to house P. gingivalis (2). Additionally it is not often found in healthy tissue, and the depth of the surface pits it forms from infection is strongly correlated to numbers of P. gingivalis present at the site (2). The bacteria cannot be found in the environment, due to its specific metabolic requirements, It can however be cultured on a blood agar plate (2).

Genome structure

The P. Gingivalis strain, 2561T has a total of 41 sequences in its genome (1). The longest among these is 9878 base pairs long and codes for a DnaK operon, the total genome is 2354886 base pairs long (1). Of these genes, 6 of them are related to 16RNA in some form. A number of the others DNA sequences are related to the virulence factors required for pathology, particularly fimbriae for which 7 of the genes code for (1). A literature review found no evidence of plasmids of any sort within the genome of P. gingivalis. Furthermore, it was confirmed that they have no cryptic plasmids, however researchers have succeeded in introducing plasmids to their genome (3). Other researchers sequenced the entire genome of strain TDC60, which is a particularly virulent strain, and found that it had a single circular genome 2339898 bp long, indicating no plasmids were present (4).

Cell structure and metabolism

P. gingivalis is a gram negative, rod-shaped bacteria. As a result it has a thinner cell wall with an outer membrane largely composed of LPS. It is also an obligate anaerobe. On account of this, as well as its niche environment on the gingiva, it has a number of adapted metabolic pathways to enable growth. One of the main features is that it requires iron from heme for growth, which it can sequester from its host using gingipains (5). Additionally, P. gingivalis cannot grow without vitamin K. the bacteria is asaccharoltyic, meaning that it can’t break down sugars. This is not necessary because the environments it lives in are often lacking in sugars. Such as within the pits it forms, at the bottom of which minimal sugars are present, therefore it produces energy by breaking down amino acids (2).

Ecology

P. gingivalis makes up a major component of the human oral microbiome, and has successfully colonised the epithelial cells of the gingiva(6). It is a compulsively anaerobic species, so cannot survive in the presence of oxygen. It can often be found in what is termed a ‘red complex’ in conjunction with Treponema denticola, and Tannerella forsythia. This complex is strongly associated with periodontal disease (7). Despite its well-researched connection with PATHOLOGY, P. gingivalis is found in numbers of patients not displaying clinical pathology (6). In general, bacteria colonising the mouth are tolerant towards and tolerated by the immune system, because inflammation leading to loss of teeth will eventually kill both the host and the bacteria (8). This is why some of the bacteria do not produce a negative reaction in the host. P. gingivalis colonises epithelial cells in the gingival compartment, which sometimes detect the bacteria and release inflammatory cytokines, however no particular apoptosis is noted in colonised cells (6). The bacteria is able to adhere to the epithelial cells due to its fimbriae, and enter the cells by binding to the β1 integrin receptor (6). It is capable of intracellular replication. Infected cells as with colonised cells do not display apoptosis, as the typical apoptotic pathways are inhibited by P. gingivalis while it replicates. In this way the bacteria is able to maintain viability within the epithelial cells for large amounts of time (6). The mouth seems to be the only habitat that this bacteria can survive in, as there is no evidence of free-living P. gingivalis (8). This makes sense, as the bacteria has very restrictive metabolic requirements. It is also suggested that the surface of the tooth may be required for colonisation, which is another factor reducing the ability of P. gingivalis to replicate outside the oral cavity. The evidence supporting this hypothesis is that the bacteria has not been cultured from edentulous babies or elderly (8). Other mammalian species are colonised by P. gingivalis, however the strains are genetically dissimilar and distinct.

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

References examples

1. Sahm, K., MacGregor, B.J., Jørgensen, B.B., and Stahl, D.A. (1999) Sulphate reduction and vertical distribution of sulphate-reducing bacteria quantified by rRNA slotblot hybridization in a coastal marine sediment. Environ Microbiol 1: 65-74.

2. Human Oral Microbiome

3. Honda, T., Takahashi, N., Miyauchi, S., yamazaki, K. (2012) Porphyromonas gingivalis lipopolysaccharide induces miR-146a without altering the production of inflammatory cytokines. Biochemical and Biophysical Research Communications 2.

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This page is written by Thomas Clarkson for the MICR3004 course, Semester 2, 2016