**Background of BPI Antibodies**
Bactericidal/Permeability-Increasing Protein (BPI) is a 45-55 kDa cationic antimicrobial protein primarily produced by neutrophils and epithelial cells. It plays a critical role in innate immunity by neutralizing gram-negative bacteria through binding to lipopolysaccharides (LPS), disrupting membrane integrity, and promoting bacterial clearance. BPI also modulates inflammatory responses by sequestering endotoxins, thereby reducing LPS-induced immune activation.
BPI antibodies, including autoantibodies against BPI, have gained attention in autoimmune and chronic inflammatory conditions. In autoimmune diseases, such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, anti-BPI antibodies are detected in a subset of patients, particularly those with granulomatosis with polyangiitis (GPA). These antibodies may impair BPI’s bactericidal function, potentially exacerbating infections or inflammation. Notably, anti-BPI antibodies are also linked to cystic fibrosis (CF), where chronic bacterial colonization (e.g., *Pseudomonas aeruginosa*) may trigger their production, contributing to persistent lung damage.
Clinically, anti-BPI antibodies are measured via ELISA or immunoassays, though their diagnostic utility remains debated due to variable prevalence across diseases. Research suggests they may serve as biomarkers for disease progression or infection risk in specific cohorts. However, their pathogenic role—whether directly damaging or epiphenomenal—requires further elucidation. Understanding BPI-antibody interactions could inform therapeutic strategies, such as targeting BPI pathways or modulating antibody production in chronic inflammatory states.