Sandwich ELISA, Biotin-labelled antibody
Serum, Plasma-EDTA, Plasma-Citrate
At ambient temperature. Upon receipt, store the product at the temperature recommended below.
Store the kit at 2–8°C. Under these conditions, assay components are stable till the expiry date is over. (See the expiry date indicated on the kit label).
Limit of Detection
n = 8; CV = 2,2%
n = 5; CV = 5,6%
- It is intended for research use only
- The total assay time is less than 3.5 hours
- The kit measures LBP in serum, plasma (EDTA, citrate)
- Assay format is 96 wells
- Standard is recombinant protein based
- Components of the kit are provided ready to use, concentrated or lyophilized
Immune Response, Infection and Inflammation, Sepsis
Lipopolysaccharide binding protein (LBP, LPS-binding protein) is a serum glycoprotein belonging to the family of lipid-binding proteins which includes also bactericidal/permeability-increasing protein (BPI), phospholipid ester transfer protein (PLTP), and cholesterol transfer protein (CLTP).
LBP is 58 kDa glycoprotein consisting of 456 amino acid residues preceded by a hydrophobic signal sequence of 25 residues. LBP is synthesized by hepatocytes and intestinal epithelial cells. Serum concentrations of LBP range between 5 and 10 ug/ml during homeostasis, increasing up to 200 ug/ml during the acute-phase response in the course of infection.
LBP expression and function are strongly associated with recognition and control of bacterial infection. LBP is an acute-phase reactant. As a class I acute-phase protein, LBP is induced by pro-inflammatory cytokines such as interleukins 1 and 6, tumor necrosis factor-alpha (TNF-α), and glucocorticoid hormones in liver and in non-hepatic tissues such as the gut and the lung.
LBP binds lipopolysaccharide (LPS, endotoxin) is released into the bloodstream during microbial infections. LBP binds to the lipid A moiety, the covalently linked lipid component of LPS. C-terminal part of LBP mediates the catalytic transfer of monomeric LPS to membrane-bound CD14, resulting in LPS-induced activation of monocytes and macrophages. LPS is released from CD14 in the lipid bilayer and binds to a complex of receptors including Toll-like receptor 4 (TLR-4) to initiate intracellular signaling cascades and transcription of genes mediated through NF-κB.
If dysregulated, these host reactions can have inadvertent outcomes such as severe sepsis, septic shock, or systemic inflammatory response syndrome (SIRS).
Several studies indicate that serum levels of LBP are significantly increased in patients with SIRS and septic shock. Serum levels of LBP have been observed to be lower in patients with SIRS than in those with septic shock.
LBP binds LPS in various pathologic states including obesity and insulin resistance, which are recognized as leading clinical conditions associated with endotoxemia. Metabolic endotoxemia has been shown to be the primary contributor to pathogenesis of chronic low-grade inflammation, characterized by increased plasma LBP levels, which are believed to originate from changes in gut microbiota and increasing intestinal permeability.