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

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].
It is recommended to prepare a solution with concentration ≥2 mg/mL. Vortex thoroughly for more than 10 minutes. Due to the adsorption characteristics of LPS, silanized container or low adsorption centrifuge tubes should be used for aliquoting and storage, and mix thoroughly before use.

TLR-4^[2]

Note:
Concentration and Time: Please do not rely solely on a single article to determine experimental conditions. It is recommended to review relevant literature based on the cell line and type of LPS before formal experiments, as the required induction time or optimal concentration for different inflammatory factors to reach their peak may vary. It is advisable to set concentration and time gradients to identify the optimal experimental scheme.
Detection Indicators: LPS does not necessarily induce cell death; therefore, it is not appropriate to determine the LPS modeling concentration and time solely by assessing cell viability. It is recommended to measure the expression or secretion of inflammatory factors.
Solvent Selection: Literature indicates that certain concentrations of DMSO can significantly inhibit LPS-induced inflammatory responses. In cellular experiments, it is recommended to prepare stock solutions using sterile water, followed by dilution with culture medium.
Container Selection: Due to the adsorption characteristics of LPS, it can bind to plastics and certain types of glass (especially at concentrations <0.1 mg/mL). The adsorption effect is relatively small when LPS concentrations exceed 1 mg/mL. Additionally, LPS tends to form micelles in solution. Therefore, when dissolving the powder, it is recommended to prepare concentrations of ≥2 mg/mL, and to vortex thoroughly for more than 10 minutes. If necessary, ultrasonic assistance may be used. For storage, please use silanized containers or low-adhesion centrifuge tubes. If glass containers are used, ensure to mix thoroughly for at least 30 minutes prior to use to re-dissolve any LPS adsorbed to the wall of the container.
Concentration Units: LPS does not have a uniform molecular weight because its molecules exhibit heterogeneity and aggregation. The molecular weight of naturally sourced LPS typically ranges from 10-100 kDa or even higher. Common dosing concentrations for LPS found in the literature are in terms of mass concentration, such as ng/mL and μg/mL, so it is sufficient to prepare solutions directly in mass concentration during experiments.
Filtration Sterilization: After dissolving LPS powder in water, saline, or PBS, the solution may appear turbid or colloidal, and in some cases, a microsphere distribution with diameters around 20-30 nm may be observed. When sterilizing by filtration, do not filter the stock solution directly. It is recommended to dilute to working solution first and then filter sterilize through a 0.22 μm filter membrane.
Differences Among Different Strain LPS: LPS of different catalog numbers comes from various bacterial strains, corresponding to different structural features such as lipid A, core polysaccharides, and O-antigens, which in turn affect the intensity of inflammation induction and TLR4-mediated signaling bias. Commonly referenced LPS catalog numbers for in vitro or in vivo inflammation model construction include HY-D1056 and HY-D1056A1. Moreover, in specific research contexts, specialized sources of LPS related to the studied bacterial strains may also be used. For example, HY-D1056D (from Porphyromonas gingivalis) is used in periodontal studies, while HY-D1056B3 (from Klebsiella pneumoniae) is relevant in pneumonia-related research. When selecting LPS, considerations should include the purpose of the experiment, sensitivity of the cell line, and other factors.

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.

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

Solid

White to off-white

[Lipopolysaccharides, from P. gingivalis]

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Gölz L, et al. Hypoxia and P. gingivalis synergistically induce HIF-1 and NF-κB activation in PDL cells and periodontal diseases. Mediators Inflamm. 2015;2015:438085.  [Content Brief]

  [2]. Park J, et al. Fucoidan inhibits LPS-induced inflammation in vitro and during the acute response in vivo. Int Immunopharmacol. 2017 Feb;43:91-98.  [Content Brief]

  [3]. Chang PC, et al. Irradiation by light-emitting diode light as an adjunct to facilitate healing of experimental periodontitis in vivo. J Periodontal Res. 2013 Apr;48(2):135-43.  [Content Brief]

  [4]. Zhang J, et al. Porphyromonas gingivalis lipopolysaccharide induces cognitive dysfunction, mediated by neuronal inflammation via activation of the TLR4 signaling pathway in C57BL/6 mice. J Neuroinflammation. 2018 Feb 9;15(1):37.  [Content Brief]