Porphyromonas gingivalis: Difference between revisions
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3.) | 3.) University at Buffalo (2007, May 9). Molecule That Destroys Bone Also Protects It, New Research Shows. ScienceDaily. Retrieved April 2, 2008, from [http://www.sciencedaily.com /releases/2007/05/070508200406.htm] | ||
In autoimmune disease, a constituent known as IL-17 is accepted to be the main cause of bone destruction and inflammation. It has been learned that in addition to causing rheumatoid arthritis (RA) this compound IL-17 is also efficient in defensive action against bacteria such as P. gingivalis, and so it helps protect the bones located in the oral cavity. A research experiment was carried out using mice. They use mice lacking the receptors for IL-17 and others used mice with receptors hindered for IL-17; these experiments assumed that the hindered receptors was a therapeutic way for the RA, as well as other diseases such as multiple sclerosis, colitis, psoriasis and lupus. To determine the effects on periodontal disease, the experiment was conducted using the mice lacking the receptors and as a result it was found that these mice were more likely to bone loss, and thus developing the disease. The effects learned were not the ones expected by researchers. In addition, a distinction between periodontal disease and an autoimmune disease should be made. A periodontal disease, is one in which it is considered an infectious disease, here leukocytes, have neutrophils as the major fighters of the infection. The IL-17 component is one of the determining factors of the regulation of neutrophils. Thus if an individual has a deficiency or is lacking the neutrophils it will lose most of its teeth due to the powerful emergence periodontal disease. The benefit of this researched experiment is that now researchers have discovered that there are more than twp types of T helper cells that contribute to the activities of the immune system. This IL-17 component is a type of T-cell “a cytokine, a protein hormone made by "T helper" cells of the immune system that stimulate immunity” which contributes to the autoimmune diseases. More research will be conducted in order to eradicate such autoimmune diseases, which harm their hosts. | In autoimmune disease, a constituent known as IL-17 is accepted to be the main cause of bone destruction and inflammation. It has been learned that in addition to causing rheumatoid arthritis (RA) this compound IL-17 is also efficient in defensive action against bacteria such as P. gingivalis, and so it helps protect the bones located in the oral cavity. A research experiment was carried out using mice. They use mice lacking the receptors for IL-17 and others used mice with receptors hindered for IL-17; these experiments assumed that the hindered receptors was a therapeutic way for the RA, as well as other diseases such as multiple sclerosis, colitis, psoriasis and lupus. To determine the effects on periodontal disease, the experiment was conducted using the mice lacking the receptors and as a result it was found that these mice were more likely to bone loss, and thus developing the disease. The effects learned were not the ones expected by researchers. In addition, a distinction between periodontal disease and an autoimmune disease should be made. A periodontal disease, is one in which it is considered an infectious disease, here leukocytes, have neutrophils as the major fighters of the infection. The IL-17 component is one of the determining factors of the regulation of neutrophils. Thus if an individual has a deficiency or is lacking the neutrophils it will lose most of its teeth due to the powerful emergence periodontal disease. The benefit of this researched experiment is that now researchers have discovered that there are more than twp types of T helper cells that contribute to the activities of the immune system. This IL-17 component is a type of T-cell “a cytokine, a protein hormone made by "T helper" cells of the immune system that stimulate immunity” which contributes to the autoimmune diseases. More research will be conducted in order to eradicate such autoimmune diseases, which harm their hosts. | ||
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Classification
Higher order taxa
Domain:Bacteria
Phylum:Bacteroidetes
Class:Bacteroides
Genus:Porphyromonas gingivalis
Species
Genus species:Porphyromonas gingivalis
Description and significance
Porphyromonas gingivalis is an anaerobic, gram negative bacterium that can be found within the mouth of an individual. It is observed to be non-motile and rod-shaped. This bacterium is the principal source of periodontal disease. It has been found that in addition to causing human infections, this bacterium also causes much of the antibiotic resistance problems found today. [1] The way which it operates is very unique, since it is a gram negative bacteria, it can attach to the subgingival coating of the tooth, and it will substitute the gram positive bacteria that is originally there with its own thus causing an inflammation which will disengage the gums from the teeth. When colonized on blood agar it forms black spots. It is important to sequence the genome of this organism because it is found in many locations within the body not only in the oral cavity also in the gastrointestinal tract, respiratory tract and in the colon, this has many consequences. It has been ascertain that periodontal disease is associated with cardiovascular diseases [2] This bacterium is associated with Treptonema denticola and Bacteroides forsythus [3]
Genome structure
The genome of p. gingivalis is circular and its origin of replication is located at oriC which is juxtaposed by the genes dnaA and PG1949. The guanine and cytosine nucleotides make up approximately 49%. At the present, 2,015 genes have been acknowledged with a total of 23,43,479 nucleotides. It has been found that the genome of p. gingivalis is similar to that of Bacteroides thetaiotaomicron, and B.fragilis within the Cytophaga-Flavobacteria-Bacteroides genome. In addition, it closely resembles the genomes of Chlorobium tepidum, and thus this demonstrates the notion that the phyla of Chlorobia and Cytophaga-Flavobacteria-Bacteroides are associated with one another. It has been discovered using genome analysis that this bacterium can metabolize a range of amino acids which will form different metabolic end products that are lethal to the host which is usually human, as well as harming the host’s gingival tissues, thus causing the expansion of periodontal disease. [4] It is found that the size of the genome of P. gingivalis is 2.34 mega bases. In addition, the sequencing of the entire genome is important to be able to determine if there are more medical effects of the bacterium in addition to periodontal disease. Researchers want to be able to establish mechanisms for the virulence as well as vaccines. The goals of this project include, the DNA sequence for the genome; analyzing and interpreting the sequence for the W83 strain; integrate the information that was obtained by the interpreted sequences and compare it with the experimental data from the P. gingivalis research community; finally the purpose of the genome sequences is to be able to make clones, reagents, and information to the research community available.[5]
Cell structure and metabolism
The P.gingivalis is a gram-negative, non-motile, rod-shaped, anaerobic organism. To function, it undergoes a mechanism in which it binds to the subgingival layer of the mouth using fimbriae. These fimbriae not only aid in the role of adhesion but are also found to be pathogenic to the immune system. [6] P. gingivalis takes part in Iron Transport, the way it does this is by using a hemin as a device to help it transport iron. When this builds up it results in the black pigmentation that is detected. To bring the hemin iron complex into the cell it uses an ABC Transporter. In regards to the metabolism P. gingivalis, it can undergo many different types such as:
Carbohydrate Metabolism:
Glycolysis / Gluconeogenesis
Citrate cycle (TCA cycle)
Pentose phosphate cycle
Pentose and glucuronate interconversions
Fructose and mannose metabolism
Galactose metabolism
Ascorbate and aldarate metabolism
Pyruvate metabolism
Glyoxylate and dicarboxylate metabolism
Propanoate metabolism
Butanoate metabolism
C5-Branched dibasic acid metabolism
Energy Metabolism:
Oxidative phosphorylation
ATP synthase
Methane metabolism
Carbon fixation
Reductive carboxylate cycle (CO2 fixation)
Nitrogen metabolism
Sulfur metabolism
Lipid Metabolism:
Fatty acid biosynthesis
Fatty acid metabolism
Synthesis and degradation of ketone bodies
Sterol biosynthesis
Bile acid biosynthesis
C21-Steroid hormone metabolism
Androgen and estrogen metabolism
Nucleotide Metabolism:
Purine metabolism
Pyrimidine metabolism
Nucleotide sugars metabolism
Amino Acid Metabolism:
Glutamate metabolism
Alanine and aspartate metabolism
Glycine, serine and threonine metabolism
Methionine metabolism
Cysteine metabolism
Valine, leucine and isoleucine degradation
Valine, leucine and isoleucine biosynthesis
Lysine biosynthesis
Lysine degradation
Arginine and proline metabolism
Histidine metabolism
Tyrosine metabolism
Phenylalanine metabolism
Tryptophan metabolism
Phenylalanine, tyrosine and tryptophan biosynthesis
Urea cycle and metabolism of amino groups
Metabolism of Other Amino Acids:
beta-Alanine metabolism
Taurine and hypotaurine metabolism
Aminophosphonate metabolism
Selenoamino acid metabolism
Cyanoamino acid metabolism
D-Glutamine and D-glutamate metabolism
D-Arginine and D-ornithine metabolism
D-Alanine metabolism
Glutathione metabolism
Metabolism of Complex Carbohydrates:
Starch and sucrose metabolism
Biosynthesis and degradation of glycoprotein
Aminosugars metabolism
Lipopolysaccharide biosynthesis
Peptideglycan biosynthesis
Glycosaminoglycan degradation
Metabolism of Complex Lipids:
Glycerolipid metabolism
Inositol phosphate metabolism
Sphingophospholipid biosynthesis
Phospholipid degradation
Sphingoglycolipid metabolism
Prostaglandin and leukotriene metabolism
Metabolism of Cofactors and Vitamins:
Thiamine metabolism
Riboflavin metabolism
Vitamin B6 metabolism
Nicotinate and nicotinamide metabolism
Pantothenate and CoA biosynthesis
Biotin metabolism
Folate biosynthesis
One carbon pool by folate
Retinol metabolism
Porphyrin and chlorophyll metabolism
Ubiquinone biosynthesis
Ecology
The organism P. gingivalis is usually found in the orifice of mammals usually humans. It is associated with Treptonema denticola and Bacteroides forsythus. There is no valid evidence that the relationship is symbiotic, but is still under researched theory. It contributes to the formation of gingivitis which is a periodontal disease.
Pathology
The bacteria, P. gingivalis, in addition to others causes gingivitis as well as periodontis. Gingivitis is "A disorder involving inflammation of the gums; may affect surrounding and supporting structures of the teeth." [7] Periodontis is "inflammatory reaction of the tissues surrounding a tooth (periodontium), usually resulting from the extension of gingival inflammation into the periodontium." [8] When a gathering of gram-negative, anaerobic bacteria is observed on the gums, it develops a biofilm called plaque on the tooth. Such bacteria as P. gingivalis and Actinobacillus actinomycetemcomitans are examples. Thus P. gingivalis expresses proteolytic enzymes which regulate the protein function in the body [9]these enzymes that are usually utilized for Cysteine and Arginine metabolism. However, here they affect the link between the tooth and the bone, thus ultimately separating the two from one another, which causes the taking apart of the tooth from jaw. [10]
Symptoms include:[11]
Swelling, redness, and pain in the gums
Bad Breath
Gums fail to have structure
Inflammation of gums
Application to Biotechnology
Does this organism produce any useful compounds or enzymes? What are they and how are they used?
Current Research
1.) [12] León R, Silva N, Ovalle A, Chaparro A, Ahumada A, Gajardo M, Martinez M, Gamonal J. "Detection of Porphyromonas gingivalis in the amniotic fluid in pregnant women with a diagnosis of threatened premature labor" International Journal of Systematic and Evolutionary Microbiology. 2007 Jul;78(7):1249-55.
It has come to the attention of researchers that pregnant women who are expected to have a premature delivery may be caused due to periodontal disease caused by the bacterium P. gingivalis. The notion that bacterial infection causes premature delivery is a common diagnosis. In an experiment with twenty-six women the amniotic sac fluid was gathered as well as sampled of the plaque that resided in the oral cavity on the subgingival layer. After doing many tests on both samples, it was found that indeed the colonies present were that of P. gingivalis. In addition this bacterium was found in the amniotic fluid. As a result of the experiments, of the twenty-six women eight of them had the speculated disease: gingivitis, twelve of them had chronic periodontitis, and the remaining six did not have symptoms of periodontal disease. Thus, women who are pregnant, or are bearing in mind pregnancy, should take care of their “oral health,” making sure that they do not develop such strains of bacteria, to prevent harm to their future offspring.
2.) [13]
It has come to the attention of researchers to investigate whether or not gum disease is associated with cardiovascular disease. In an experiment, they took four strains of P. gingivalis and permitted them to contaminate and live inside the artery cells. In a previous experiment Paulo Rodrigues, and his fellow researchers had determined that this bacterium P. gingvalis is able to “invade and survive inside human artery cells.” Thus in this new experiment, after the four strains were developed, they then mutated a gene in each thus seeking to see if with now a “disability” if the bacterium could still “invade and survive” inside the artery cells. After running the tests, it was found that because the strains were now mutated they couldn’t invade as effectively and their survival rate was lessened. This is very important because now we can keep in mind that this pathogenic bacteria is linked with the artery cells, and with further study we may be able to develop “tools” for the averting cardiovascular diseases.
3.) University at Buffalo (2007, May 9). Molecule That Destroys Bone Also Protects It, New Research Shows. ScienceDaily. Retrieved April 2, 2008, from /releases/2007/05/070508200406.htm
In autoimmune disease, a constituent known as IL-17 is accepted to be the main cause of bone destruction and inflammation. It has been learned that in addition to causing rheumatoid arthritis (RA) this compound IL-17 is also efficient in defensive action against bacteria such as P. gingivalis, and so it helps protect the bones located in the oral cavity. A research experiment was carried out using mice. They use mice lacking the receptors for IL-17 and others used mice with receptors hindered for IL-17; these experiments assumed that the hindered receptors was a therapeutic way for the RA, as well as other diseases such as multiple sclerosis, colitis, psoriasis and lupus. To determine the effects on periodontal disease, the experiment was conducted using the mice lacking the receptors and as a result it was found that these mice were more likely to bone loss, and thus developing the disease. The effects learned were not the ones expected by researchers. In addition, a distinction between periodontal disease and an autoimmune disease should be made. A periodontal disease, is one in which it is considered an infectious disease, here leukocytes, have neutrophils as the major fighters of the infection. The IL-17 component is one of the determining factors of the regulation of neutrophils. Thus if an individual has a deficiency or is lacking the neutrophils it will lose most of its teeth due to the powerful emergence periodontal disease. The benefit of this researched experiment is that now researchers have discovered that there are more than twp types of T helper cells that contribute to the activities of the immune system. This IL-17 component is a type of T-cell “a cytokine, a protein hormone made by "T helper" cells of the immune system that stimulate immunity” which contributes to the autoimmune diseases. More research will be conducted in order to eradicate such autoimmune diseases, which harm their hosts.
References
1. <|Disease Database>
2. <| Wikipedia>
3. ScienceDaily 6 July 2007. 2 April 2008 http://www.sciencedaily.com/releases/2007/07/070703171912.htm
5. Bacterium To Invade Arteries. ScienceDaily. Retrieved April 2, 2008, from http://www.sciencedaily.com/releases/2006/05/060529082223.htm