lipopolysaccharide

Biotin-Lipopolysaccharide, fromE.coliO111:B4, is a biotin-conjugated Lipopolysaccharide (LPS) capable of binding with streptavidin proteins. Biotin-Lipopolysaccharide, fromE.coliO111:B4, can be utilized for the identification of Lipopolysaccharide ligands.

Lipopolysaccharides (LPS), derived from Escherichia coli O55:B5, are essential components of the outer membrane of Gram-negative bacteria. Composed of lipid A, a core oligosaccharide, and an O-specific polysaccharide, LPS exhibits strong immunogenicity. It activates immune cells via the TLR4 receptor, induces chemotactic cell migration and cytokine secretion, and helps maintain the integrity of the bacterial outer membrane, protecting against bile salts and lipid-based antibiotics. LPS is commonly used to establish inflammatory models, including arthritis, chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), and gastrointestinal disease models.

Lipopolysaccharides, from Proteus vulgaris, are endotoxins sourced from the bacterium Proteus vulgaris, functioning as TLR-4 activators and representing S-type LPS. They play a role in activating pathogen-associated molecular patterns (PAMP) and stimulate cells to secrete migration-inducing agents. This lipopolysaccharide displays a characteristic three-part structure: O antigen, core oligosaccharide, and lipid A. Furthermore, it has a unique molecular configuration and a chitosan affinity (Kb=2.72 μM), which is superior to that of Yersinia pseudotuberculosis (Kb=6.06 μM) and Escherichia coli (Kb=79.50 μM).

Lipopolysaccharides from *Salmonella enterica* serotype Abortusequi are endotoxins and TLR-4 activators derived from intestinal S. enterica. They are mutated R-type LPSs that serve as pathogen-associated molecular patterns (PAMP) to activate the immune system and induce cell secretion of exosomes. These lipopolysaccharides consist of a core oligosaccharide and lipid A. *S. enterica* serotype Abortusequi is a key pathogen causing abortion in mares and is associated with neonatal septicemia, multiple abscesses, orchitis, and polyarthritis in equine species. Grouping is primarily based on lipopolysaccharide (O-antigen) and flagellin protein (H-antigen).

Lipopolysaccharides are endotoxins composed of lipopolysaccharide structures and serve as TLR-4 activators, triggering pathogen-associated molecular patterns (PAMP) of the immune system and inducing cellular secretion of vesicles. Extracted from the outer leaflet of the outer membrane of Gram-negative bacteria, they consist of an O-antigen-specific chain, a core oligosaccharide, and lipid A. Lipopolysaccharides, from P. gingivalis, refer specifically to the endotoxin derived from Porphyromonas gingivalis.

Lipopolysaccharides from P. aeruginosa (Pseudomonas aeruginosa) 10 are endotoxins and TLR4 activators that originate from the bacterium P. aeruginosa 10, classified as S-type LPS. They exhibit a characteristic tripartite structure: an O antigen, a core oligosaccharide, and lipid A. The lipopolysaccharides from P. aeruginosa 10 are distinct due to their unique fatty acid composition, an unusually high level of phosphorylation (identified as triphosphate residues), and a distinctive outer region in the core oligosaccharide. Moreover, their O-specific side chains are typically rich in novel amino sugars. These lipopolysaccharides display susceptibility to viruses, with their viral sensitivity being influenced by the molecular weight polysaccharide content. A reduction in high-molecular-weight polysaccharides increases their sensitivity to bacteriophages.

Lipopolysaccharides from *E. coli* (Escherichia coli) O26:B6 are endotoxins derived from *E. coli* that function as TLR-4 activators. These S-type LPS molecules can trigger pathogenic-associated molecular patterns (PAMP) and encourage the release of exosomes. Structurally, they are composed of three parts: O-antigen, core oligosaccharide, and Lipid A, and can be identified by the monoclonal antibody MAb J8-4C10. This compound can increase pro-inflammatory cytokines in plasma, leading to activation of the hypothalamic-pituitary-adrenal (HPA) axis and causing oxidative damage to the adrenal glands. However, the pathogenic activity of Lipopolysaccharides from *E. coli* O26:B6 can be inhibited by PD149163 .

Lipopolysaccharides, from S. marcescens (Serratia marcescens), are endotoxins derived from the bacterium Serratia marcescens, functioning as TLR-4 activators and classified as S type LPS. These compounds activate the immune system through pathogen-associated molecular patterns (PAMPs) and stimulate the secretion of chemokines. They feature a typical tripartite structure consisting of the O-antigen, core oligosaccharide, and Lipid A. Lipopolysaccharides from S. marcescens promote NF-κB activation in mouse cells via Toll-like receptor (TLR4)/MD-2 pathways. Additionally, these lipopolysaccharides can induce apoptosis in host immune cells, thereby suppressing the host's innate immunity.

Lipopolysaccharides from E. coli O127:B8 (LPS, from Escherichia coli (O127:B8)) are endotoxins and TLR-4 activators extracted from the bacterium E. coli O127:B8. This smooth (S) type LPS features a typical tripartite structure: an O antigen, an R3 core oligosaccharide, and lipid A. When lipopolysaccharides from E. coli O127:B8 activate TLR-4 on immune cells, they can trigger inflammatory responses and ileal contractility, making them useful for developing intestinal inflammation models.

Lipopolysaccharides, fromProteus mirabilis, are endotoxins derived from the bacterium Proteus mirabilis, functioning as TLR-4 activators and featuring an S-type LPS structure. They play a role in activating pathogen-associated molecular patterns (PAMP) and inducing cell-extracellular vesicle release. These lipopolysaccharides have a classic tripartite structure: O antigen, core oligosaccharide, and lipid A. Proteus mirabilis is a primary pathogen responsible for urinary tract infections and has potential links to rheumatoid arthritis. Additionally, Lipopolysaccharides, fromProteus mirabilis, exhibit promising antitumor effects, showing in vivo inhibitory activity against solid tumors such as meningeal sarcoma and Walker carcinoma.

Lipopolysaccharides, from Salmonella typhosa, are endotoxins and TLR-4 activators originating from Salmonella typhosa. These S-type lipopolysaccharides can stimulate the immune system's pathogen-associated molecular patterns (PAMP) and induce cellular secretion of migratory bodies. They exhibit a typical three-part structure: O antigen, core oligosaccharide, and lipid A. These lipopolysaccharides can function as vaccine adjuvants, enhancing the immune response, particularly by modulating B cell activity.

Lipopolysaccharides (LPS, from Akkermansia muciniphila) are endotoxins derived from the bacterium Akkermansia muciniphila. This lipid-polysaccharide endotoxin acts as a TLR-4 activator, triggering pathogen-associated molecular patterns (PAMP) in the immune system and inducing cell secretion of migratory factors. Lipopolysaccharides are extracted from the outer leaflet of the outer membrane of Gram-negative bacteria and consist of an antigen O-specific chain, a core oligosaccharide, and lipid A.

Lipopolysaccharides, from E. coli O128:B12 (LPS, from Escherichia coli [O128:B12]) are lipid polysaccharide endotoxins and TLR-4 activators derived from E. coli O128:B12, characterized as a smooth (S) type LPS. This compound features a typical three-part structure: O antigen, R3 core oligosaccharide, and lipid A. It activates TLR-4 in immune cells, is useful for developing neonatal brain inflammation models in animals, and may impact preterm birth in neonates.

Lipopolysaccharides, from E. coli (Escherichia coli) K-235, are endotoxins derived from Escherichia coli and serve as TLR-4 activators. They are an S-type LPS capable of activating pathogen-associated molecular patterns (PAMP) of the immune system and inducing the secretion of exosomes. This compound is characterized by a typical three-part structure comprising the O-antigen, core oligosaccharide, and Lipid A. Additionally, lipopolysaccharides from E. coli K-235 stimulate mitogenesis in C57BL/10ScN spleen cells and, when purified by butanol and deoxycholate methods, can stimulate spleen cells from C57BL/10ScCR and C3H/HeJ mice.

Lipopolysaccharides, from S. enterica (Salmonella enterica) serotype enteritidis, are endotoxins derived from this serotype known for causing enteritis and serve as TLR-4 activators. This S-type LPS triggers the immune system's pathogen-associated molecular patterns (PAMP) and induces the secretion of exosomes. It consists of a typical tripartite structure: the O antigen, core oligosaccharide, and lipid A. These lipopolysaccharides can provoke a systemic inflammatory response, leading to increased plasma levels of TNF-α, IFN-γ, IL-6, IL-10, and nitrates.

Lipopolysaccharides (LPS) are specific endotoxins that serve as a major component of the cell walls in gram-negative bacteria. Composed of Lipid A, a core oligosaccharide, and an O-specific polysaccharide, LPS strongly stimulates the immune system by binding to Toll-like receptor 4 (TLR4) on immune cells, triggering inflammatory responses. In most Salmonella serotypes, the LPS features a complex O-antigen (OAg) structure, with core oligosaccharide OAg units ranging from 16 to over 100 repeats. Mutations in OAg regulatory factors can alter the OAg structure, affecting Salmonella interactions with epithelial cells. Strains with long OAgs show increased translocation and invasion by SPI1-T3SS effector proteins, while strains lacking OAg entirely exhibit increased invasiveness and adhesion. This product is derived from Salmonella enterica serotype minnesota and is utilized for studies on host immune activation and its roles in inflammation and immune modulation.

Lipopolysaccharides, from S. enterica (Salmonella enterica) serotype typhimurium, are endotoxins and TLR4 activators derived from the serotype of this bacterium, classified as S-type LPS. They display a characteristic three-part structure: O antigen, core oligosaccharide, and lipid A. These lipopolysaccharides influence bacterial fate within dendritic cells (DC), determining the uptake, degradation, and activation of immune functions in DC cells.

Nisin Z has anti-inflammatory activity and reduces pro-inflammatory cytokine release by inhibiting activation of the ERK1/2 and p38 mitogen-activated protein kinase (MAPK) signaling pathways, attenuating lipopolysaccharide-induced mastitis through inhibition of the ERK1/2 and p38 mitogen-activated protein kinase signaling pathways.

Lipid A-11 is a lipid component of endotoxin that is primarily responsible for the toxic properties of gram-negative bacteria. Lipid A-11 constitutes the innermost region of the lipopolysaccharide (LPS) molecule, also known as endotoxin, and its hydrophobic nature facilitates anchoring of the LPS structure into the bacterial outer membrane. Lipid A-11 plays a critical role in host-pathogen interactions, contributing to septic shock and immunological activation during bacterial infections.

2-Hydroxydecanoic acid ((±)-α-hydroxy Decanoic Acid) is a fatty acid found in the lipophilic portion of the lipopolysaccharide fraction of the aerobic bacterium P. ovalis.

(Z)-KC02 is an ABHD16A inhibitor which targets the enzyme responsible for producing lysophosphatidylserine (lyso-PS), a lipid involved in regulating immune and neurological functions. This compound is linked to the mitigation of neurological disorders, including retinitis pigmentosa and cataracts (PHARC), by depleting lyso-PS in lymphoblasts from affected individuals. Moreover, (Z)-KC02 diminishes lyso-PS levels and lipopolysaccharide-induced cytokine production in macrophages and influences lyso-PS metabolism in vivo [1].