Lipopolysaccharide (LPS), specifically the Lipid A component (LPS for lipopolysaccharide; Lipid A (no standard single abbreviation))

Lipopolysaccharide (LPS) is a complex glycolipid forming the outer leaflet of Gram-negative bacterial outer membranes, composed of three main domains: O-antigen, core oligosaccharide, and the lipid A moiety[5][7][9]. Lipid A is a phosphorylated glucosamine disaccharide with multiple fatty acyl chains, and is chiefly responsible for the toxic effects of LPS, causing fever, shock, and strong immune responses when recognized by host cells via the Toll-like receptor 4 (TLR4)[1][4][8][3]. Its precise structure and acylation pattern vary among species, modulating both immune activation and antimicrobial susceptibility[1][7]. Lipid A biosynthesis is highly conserved and essential for bacterial viability, making it an attractive but challenging target for therapeutic intervention. Drugs such as polymyxins, TLR4 antagonists, and detoxifying enzymes have been developed to modulate its effects, especially in combating Gram-negative bacterial infections and sepsis[8][4][1].

Other names

endotoxinLPSlipooligosaccharide (variants)LPS coreLipid ALPS lipid A domainbacterial endotoxin

Direct binding and neutralization of Lipid A (polymyxins); Competitive antagonism of TLR4 receptor activation (Lipid A analogs like eritoran); Enzymatic detoxification (dephosphorylation by alkaline phosphatase, removal of acyl chains by AOAH enzyme)