SMB00610
Lipopolysaccharide from Porphyromonas gingivalis
purified by phenol extraction
Synonym(s):
LPS
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About This Item
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biological source
Porphyromonas gingivalis
Quality Level
form
powder
purified by
phenol extraction
impurities
≤3% Protein (Lowry)
color
white to faint yellow
solubility
triethylene glycol dimethyl ether: 0.90-1.10 mg/mL to hazy, colorless to light yellow
shipped in
ambient
storage temp.
2-8°C
General description
Lipopolysaccharides (LPSs) are characteristic components of the cell wall of Gram-negative bacteria like Porphyromonas gingivalis. It differs from LPS from Escherichia coli in its structure and various functional activities.
Application
Lipopolysaccharide has been used:
- as a treatment to stimulate acute lung injury in human bronchial epithelial (HBE) cells
- as an agonist for toll-like receptor 4 (TLR4) and to stimulate intestinal normal fibroblasts (NFs) to study osteopontin (OPN) expression in myofibroblasts
- to study its effects on pro-inflammatory and pro-coagulant genes expression in endothelial cells
Biochem/physiol Actions
LPS and its lipid A moiety stimulate cells of the innate immune system by the Toll-like receptor 4 (TLR4), a member of the Toll-like receptor protein family, which recognizes common pathogen-associated molecular patterns (PAMPs).
Additionally, it was demonstrated that the mechanisms by which LPS from E. coli and P. gingivalis modulate cluster of differentiation 14 (CD14), toll-like receptor 2 (TLR2), and toll-like receptor 4 (TLR4) surface expression, primary and secondary cytokine responses are different.
Porphyromonas gingivalis is a Gram-negative bacterium that is known to be involved in adult periodontitis. Periodontitis is a chronic inflammatory disease characterized by the recession of the supportive tissue surrounding teeth. Studies have shown that the LPS from P. gingivalis plays an important role in this disease.
A recent study demonstrated that LPS from P. gingivalis stimulates insulin secretion by the pancreatic β cell line, MIN6. In the presence of 5 mM glucose and 50-500 ng/mL LPS from P. gingivalis, a significant induction of insulin secretion was observed.
Additionally, it was demonstrated that the mechanisms by which LPS from E. coli and P. gingivalis modulate cluster of differentiation 14 (CD14), toll-like receptor 2 (TLR2), and toll-like receptor 4 (TLR4) surface expression, primary and secondary cytokine responses are different.
Porphyromonas gingivalis is a Gram-negative bacterium that is known to be involved in adult periodontitis. Periodontitis is a chronic inflammatory disease characterized by the recession of the supportive tissue surrounding teeth. Studies have shown that the LPS from P. gingivalis plays an important role in this disease.
A recent study demonstrated that LPS from P. gingivalis stimulates insulin secretion by the pancreatic β cell line, MIN6. In the presence of 5 mM glucose and 50-500 ng/mL LPS from P. gingivalis, a significant induction of insulin secretion was observed.
Preparation Note
LPS from P. gingivalis is soluble in water and cell culture medium DMEM (1-5 mg/mL), yielding a clear solution.
Other Notes
To gain a comprehensive understanding of our extensive range of Lipopolysaccharides for your research, we encourage you to visit our Carbohydrates Category page.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Customers Also Viewed
Differential expression of immunoregulatory genes in monocytes in response to Porphyromonas gingivalis and Escherichia coli lipopolysaccharide.
Clinical and Experimental Immunology, 156, 479-487 (2009)
Virulence factors of Porphyromonas gingivalis.
Periodontology 2000, 20, 168-238 (1999)
Innate immunity, 14(2), 99-107 (2008-08-21)
Lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis has been shown to differ from enterobacterial LPS in structure and function; therefore, the Toll-like receptors (TLRs) and the intracellular inflammatory signaling pathways are accordingly different. To elucidate the signal transduction
Epidemiology of subgingival bacterial pathogens in periodontal disease
Molecular Pathogenesis of Periodontal Disease, 1, 1-12 (1994)
Epidemiology of subgingival bacterial pathogens in periodontal disease.
Molecular Pathogenesis of Periodontal Disease, 1-12 (1994)
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