Human Bacterial/Permeability-Increasing Protein (BPI, CAP57)
Native whole molecule
Produktdetails
Synonyms
BPI, CAP57
Description of Human Bacterial/Permeability-Increasing Protein (BPI, CAP57)
Human Bacterial/Permeability-Increasing Protein (BPI, CAP57) is a 55 kDa protein. Bactericidal/Permeability-Increasing Protein (BPI) is a cationic glycoprotein stored in azurophilic granules of polymorphonuclear leukocytes (PMNs). Its boomerang-shaped structure features two functional domains: an N-terminal region (residues 1–199) responsible for antimicrobial and endotoxin-neutralizing activities, and a C-terminal domain facilitating opsonization and immune cell interactions. BPI selectively targets Gram-negative bacteria via high-affinity binding (Kd ~2–5 nM) to lipopolysaccharides (LPS), disrupting outer membrane integrity through hydrophobic pocket interactions with lipid A, leading to bacterial permeabilization and death. Additionally, BPI inhibits LPS-induced immune activation by blocking interactions with LPS-binding protein (LBP) and CD14, thereby attenuating cytokine storms. Clinically, BPI serves as a major autoantigen for anti-neutrophil cytoplasmic antibodies (ANCA) in systemic vasculitis, particularly in patients with chronic Gram-negative infections like cystic fibrosis or inflammatory bowel disease. BPI-ANCA immune complexes induce neutrophil extracellular trap (NET) formation via TNFα-primed neutrophils, exacerbating vascular inflammation and contributing to pauci-immune glomerulonephritis and cutaneous vasculitis. Elevated BPI levels (>45 ng/mL) also correlate with sepsis severity and mortality, serving as a prognostic biomarker. Therapeutically, recombinant N-terminal fragments (e.g., rBPI21) demonstrate efficacy in neutralizing endotoxin and improving survival in meningococcal sepsis models. Clinical trials highlight its potential in hemorrhagic trauma and peritoneal infections, while synthetic BPI mimetics and monoclonal antibodies targeting BPI-ANCA pathways are under investigation for vasculitis. These applications underscore BPI’s dual role as a sentinel of innate immunity and a bridge to autoimmune pathology.
Source
Neutrophils shown to be non reactive for HBsAg, anti-HCV, anti-HBc, and negative for anti-HIV 1 & 2 by FDA approved tests.
Storage
For long term, store Human Bacterial/Permeability-Increasing Protein (BPI, CAP57) at ≤ -80°C.
Applications
Antimicrobial, Inflammation, In Vitro Diagnostic, Cell based assays, ANCA related vasculitis.
Citations/Publications
Bernard, Q., et al., (2018), 'Plasticity in early immune evasion strategies of a bacterial pathogen', PNAS., 11(16): pp E3788–E3797. Available at: doi/10.1073/pnas.1718595115.
Bülow, S., et al., (2018), 'Bactericidal/Permeability-Increasing Protein Is an Enhancer of Bacterial Lipoprotein Recognition', Front. Immunol. 9: pp 2768. Available at: doi: 10.3389/fimmu.2018.02768.
Theprungsirikul, J. L., et al., (2021), 'Bactericidal/Permeability-Increasing Protein Preeminently Mediates Clearance of Pseudomonas aeruginosa In Vivo via CD18-Dependent Phagocytosis', Front. Immunol., 12: pp 659523. Available at: doi: 10.3389/fimmu.2021.659523.
Bülow, S., et al., (2024), Bactericidal/permeability-increasing protein instructs dendritic cells to elicit Th22 cell response', Cell Reports 43: pp 113929. Available at: https://doi.org/10.1016/j.celrep.2024.113929
Skopelja, S., et al., (2016), 'The role for neutrophil extracellular traps in cystic fibrosis autoimmunity', JCI Insight., 1(17): pp e88912. Available at: doi:10.1172/jci.insight.88912.
NCBI: https://www.ncbi.nlm.nih.gov/protein/P17213
Shipped with dry ice
Usage: For research use only. Not for use in diagnostic or therapeutic procedures. Not for human use.
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