1. Immunology/Inflammation
  2. Toll-like Receptor (TLR)
  3. Lipopolysaccharides, from P. gingivalis

Lipopolysaccharides, from P. gingivalis  (Synonyms: LPS, from Porphyromonas gingivalis)

Cat. No.: HY-D1056D
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Lipopolysaccharides, from P. gingivalis (LPS, from Porphyromonas gingivalis) are endotoxins and TLR4 activators extracted from Porphyromonas gingivalis (P. gingivalis) and are classified as S (smooth) type LPS. Lipopolysaccharides, from P. gingivalis possess the typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from P. gingivalis activate TLR-4 in immune cells and are important virulence factors in the mechanism of periodontal disease. Lipopolysaccharides, from P. gingivalis can be used in research related to periodontitis.

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Lipopolysaccharides, from P. gingivalis Chemical Structure

Lipopolysaccharides, from P. gingivalis Chemical Structure

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Description

Lipopolysaccharides, from P. gingivalis (LPS, from Porphyromonas gingivalis) are endotoxins and TLR4 activators extracted from Porphyromonas gingivalis (P. gingivalis) and are classified as S (smooth) type LPS. Lipopolysaccharides, from P. gingivalis possess the typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from P. gingivalis activate TLR-4 in immune cells and are important virulence factors in the mechanism of periodontal disease. Lipopolysaccharides, from P. gingivalis can be used in research related to periodontitis[1][2][3][4].

IC50 & Target

TLR-4[2]

In Vitro

Note:
To maintain the integrity of LPS, it is recommended to store LPS solution in silanized containers. This is because LPS can adhere to plastics and certain types of glass, particularly at concentrations below 0.1 mg/mL. If the LPS concentration exceeds 1 mg/mL, this adsorption effect is relatively minimal. If using glass containers, ensure that the solution is thoroughly mixed for at least 30 minutes before use to redissolve any LPS that may have adsorbed to the tube walls.

LPS is the major toxic component of Gram-negative bacteria, capable of activating pathogen-associated molecular patterns (PAMP) of the immune system and inducing cellular secretion of migrasomes. LPS can be recognized by TLR4, activating the innate immune system, followed by promoting NF-κB activation and the production of pro-inflammatory cytokines, commonly used in experiments for the stimulation, activation, and differentiation of immune cells.
Different types of bacteria express LPS with varying structures and biological activities. LPS generally comes in two configurations: R (rough) type and S (smooth) type. S-type LPS contains a typical three-part structure: O-antigen (O-antigen) (serum-specific polysaccharides composed of repeating oligosaccharide units), core oligosaccharide (core) (C9-type non-repeating oligosaccharides), and lipid A (Lipid A) (the toxic component of LPS). The R type does not contain an O-antigen and expresses rough-type LPS. The lack of O-antigen can affect how immune cells recognize LPS.
Lipopolysaccharides, from P. gingivalis are classified as S-type LPS and can induce NF-κB activation in human periodontal ligament (PDL) cells[1].
Lipopolysaccharides, from P. gingivalis (pg-LPS) (1 μg/mL; 12-24 h) upregulate iNOS and COX-2 expression in RAW 264.7 cells and increase the levels of pro-inflammatory factors TNF-α, IL-1β, and IL-6[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[2]

Cell Line: RAW 264.7 cells
Concentration: 1 μg/mL
Incubation Time: 12-24 h
Result: Enhanced the expression levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6.
In Vivo

Induction of periodontitis model[2][3][4]
Background
LPS induces a periodontitis model by simulating bacterial infection, activating immune cells to release inflammatory mediators, triggering chronic inflammation, damaging periodontal tissues and affecting bone metabolism.
Specific Modeling Methods
C57BL/6 mice • BALB/c mice • 4-10 μg; 2-4 times • Injection into the oral periodontal tissues
Note
(1) Before inducing an animal model with LPS, relevant references should be consulted based on the experimental purpose, animal type, etc., and preliminary experiments should be conducted to determine the optimal experimental protocol.
(2) After LPS administration, the time points at which the peak levels of different inflammatory factors appear may vary. It is recommended to determine the experimental protocol according to references, and multiple time points should be selected for detection during preliminary experiments.
(3) LPS should be stored away from light and avoid repeated freezing and thawing.
(4) A certain concentration of DMSO can significantly inhibit the inflammatory response induced by LPS. It is recommended to dissolve LPS in PBS or ddH2O.
Modeling Indicators
The expressions of IL-1β, IL-6, TNF-α and so on in the gingival tissues increase.
HE staining of the gingival/alveolar bone tissues: infiltration of inflammatory cells, and the collagen fiber bundles are loosely distributed near the tissue-root interface.
The number of immune cells in the gingival tissues increases.
Opposite Product(s): Fucoidan (HY-132179)

Lipopolysaccharides, from P. gingivalis induce inflammatory responses in mouse and rat models of periodontitis[2][3].
Lipopolysaccharides, from P. gingivalis (pg-LPS) (1 μg/1 mL; 4 times; oral injection) can elicit tissue inflammatory responses in mice, promote the increase of pro-inflammatory factor levels, and recruit immune cells. The inflammatory response induced by Lipopolysaccharides, from P. gingivalis can be inhibited by Fucoidan (HY-132179) (5 mg/mL, 100 μL; twice daily for 3 days)[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female BALB/c mice (6-week-old)[2]
Dosage: 1 μg in 1 μL sterile PBS
Administration: 4 times Buccal injection, via a microinjection and Hamilton N731 needle; with or without Fucoidan (HY-132179) (5 mg/mL with 2% carboxymethycellulose in 100 μL PBS), which was administered via oral topical application twice a day for 3 days after the last injection.
Result: Stimulated iNOS gene expression by 5.7-fold, which was significantly inhibited by fucoidan.
Elevated the the serum level of TNF, and resulted inflammation and inflammatory cell recruitment in mouse gingival tissue.
SMILES

[Lipopolysaccharides, from P. gingivalis]

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Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Lipopolysaccharides, from P. gingivalis
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