2. Induced Disease Models Products Immunology/Inflammation
  3. Immunology and Inflammatory Disease Models Toll-like Receptor (TLR)
  4. Lipopolysaccharides, from E. coli O111:B4

Lipopolysaccharides, from E. coli O111:B4  (Synonyms: LPS, from Escherichia coli (O111:B4))

Cat. No.: HY-D1056A1
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Lipopolysaccharides, from E. coli O111:B4 (LPS, from Escherichia coli (O111:B4)) are endotoxins and TLR4 activators extracted from Escherichia coli (E. coli O111:B4) and are classified as S (smooth) type LPS. Lipopolysaccharides, from E. coli O111:B4 possess the typical three-part structure: O-antigen, R3-type core oligosaccharide, and lipid A. Lipopolysaccharides, from E. coli O111:B4 activate TLR-4 in immune cells and can cause significant gastric diseases. Lipopolysaccharides, from E. coli O111:B4 can be used to induce cellular inflammation and establish animal models related to inflammation.

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Lipopolysaccharides, from E. coli O111:B4 Chemical Structure

Lipopolysaccharides, from E. coli O111:B4 Chemical Structure

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Lipopolysaccharides, from E. coli O111:B4 Related Antibodies

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Description

Lipopolysaccharides, from E. coli O111:B4 (LPS, from Escherichia coli (O111:B4)) are endotoxins and TLR4 activators extracted from Escherichia coli (E. coli O111:B4) and are classified as S (smooth) type LPS. Lipopolysaccharides, from E. coli O111:B4 possess the typical three-part structure: O-antigen, R3-type core oligosaccharide, and lipid A. Lipopolysaccharides, from E. coli O111:B4 activate TLR-4 in immune cells and can cause significant gastric diseases. Lipopolysaccharides, from E. coli O111:B4 can be used to induce cellular inflammation and establish animal models related to inflammation[1][2][3][4][5][6][7][8][9].

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.
E. coli expresses four LPS serotypes: O111:B4, O55:B5, O127:B8, O128:B12. The LPS expressed by the E. coli O111:B4 strain is known to cause significant gastrointestinal diseases and is the most cited LPS strain in literature. LPS derived from E. coli O111:B4 can induce polarization of human macrophages (M1)[5].

1. Induction of cellular inflammation model[6][7]
Background
LPS binds to the TLR4-MD-2 complex on the cell surface, activates both MyD88-dependent and MyD88-independent signaling pathways, promotes the translocation of transcription factors such as NF-κB into the nucleus, triggers the expression of inflammation-related genes, and leads to the occurrence of an inflammatory response in cells.
Specific Modeling Methods
Cell: Macrophages, tumor cells, glial cells and so on.
Administration: 0.1-10 μg/mL • 1-24 h
Note
(1) Before the formal experiment, relevant references should be consulted according to the cell line and the source of LPS, etc., and concentration and time gradients should be screened to determine the optimal experimental protocol.
(2) Stimulating cells with LPS does not necessarily lead to cell death. Therefore, it is not appropriate to determine the concentration and time of LPS for establishing the model merely by detecting cell viability. It is recommended to detect the expression and secretion of multiple inflammatory factors.
(3) During the process of stimulating cells with LPS, the morphological changes of cells should be observed regularly. An excessively high concentration may cause cytotoxicity, while an excessively low concentration may fail to effectively damage the cells.
(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.
(5) In the research on the construction of in vitro inflammatory models, Lipopolysaccharides, from E. coli O55:B5 (HY-D1056) and Lipopolysaccharides, from E. coli O111:B4 (HY-D1056A1) are the most widely used LPS, and they are highly recommended!
Modeling Indicators
The secretion/expression of inflammatory factors such as IL-1β, IL-6 and TNF-α in the supernatant or cells increases.
The release of NO increases.
The expression of inflammatory genes such as iNOS, NF-κB and NLRP3 increases.
Correlated Product(s) Lipopolysaccharides, from E. coli O55:B5 (HY-D1056)
Opposite Product(s): /

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

Lipopolysaccharides, from E. coli O111:B4 Related Antibodies
In Vivo

Lipopolysaccharides, from E. coli O55:B5 (HY-D1056) can be used to induce cell and animal models related to inflammation. Among them, the animal models include sepsis (shock) model, cardiac dysfunction/myocarditis model, acute lung injury model, acute liver injury model, encephalitis model, depression model, etc. The following are examples of several models:

1. Induction of septic shock/sepsis model[8]
Background
After entering the body, LPS is recognized by TLR4, which activates the relevant signaling pathways and triggers the massive release of inflammatory mediators. This, in turn, leads to a series of pathophysiological changes such as the out-of-control inflammatory response, vascular endothelial injury, and activation of the coagulation system, ultimately inducing the occurrence of sepsis (septic shock).
Specific Modeling Methods
C57BL/6 mice • 2.5-10 mg/kg • i.p.
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.
Modeling Indicators
The secretion of TNF-α, IL-6, IL-1β, etc. in the serum/plasma increases.
HE staining of the kidney: proliferation of glomerular cells, degeneration and necrosis of epithelial cells, infiltration of interstitial inflammatory cells, etc.
The levels of Scr and BUN (markers of renal filtration function) increase.
Correlated Product(s): Lipopolysaccharides, from E. coli O55:B5 (HY-D1056)
Correlated Product(s): /
2. Induction of acute liver failure model[8][9]
Background
LPS is often used in combination with D-galactosamine (D-GalN) to induce an acute liver injury model. LPS activates the immune system and triggers an inflammatory response, while D-galactosamine causes metabolic disorders in hepatocytes and increases their sensitivity to damaging factors. Through the synergistic effect of the two, acute liver injury is induced via mechanisms such as the attack of inflammatory mediators.
Specific Modeling Methods
C57BL/6 mice • 5-50 μg/kg + D-GalN (200-400 mg/kg) • i.p.
Modeling Indicators
The secretion or expression of TNF-α, IL-6 and IL-1β increases in the serum or liver tissue.
HE staining of the liver: disordered liver structure, bleeding plaques, infiltration of inflammatory cells, etc.
The levels of ALT and AST (markers of liver injury) increase significantly.
Correlated Product(s): Lipopolysaccharides, from E. coli O55:B5 (HY-D1056)
Opposite Product(s): /

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

Solid

Color

White to off-white

SMILES

[Lipopolysaccharides, from E. coli O111:B4]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 1 mg/mL (ultrasonic and warming and heat to 60°C)

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Purity & Documentation

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Handling Instructions (2659 KB)
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Lipopolysaccharides, from E. coli O111:B4 Related Classifications

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.

Keywords:

Lipopolysaccharides, from E. coli O111:B4LPS, from Escherichia coli (O111:B4)Toll-like Receptor (TLR)Inhibitorinhibitorinhibit

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