Lipopolysaccharide lipid A-phosphoethanolamine (LPS-pEtN) (LPS-pEtN)

Lipopolysaccharide (LPS) is a major structural component of the outer membrane of Gram-negative bacteria, consisting of a lipid A anchor, a core oligosaccharide, and an O-antigen (Raetz & Whitfield, 2002, Annual Review of Biochemistry). The lipid A-phosphoethanolamine region specifically refers to a modified form of lipid A where phosphoethanolamine (pEtN) groups are attached to the phosphate moieties, often mediated by the MCR-1 enzyme (Liu et al., 2016, Lancet Infectious Diseases). This modification is a primary mechanism of resistance against polymyxin antibiotics, as it reduces the negative charge of the bacterial membrane, thereby preventing the binding of cationic drugs (Baron et al., 2016, International Journal of Antimicrobial Agents). Biologically, LPS is essential for membrane stability and acts as a potent endotoxin, triggering systemic inflammatory responses through the TLR4 receptor complex (Beutler & Rietschel, 2003, Nature Reviews Immunology). In clinical settings, the presence of pEtN-modified lipid A is a critical marker for multidrug-resistant infections, particularly those involving Enterobacteriaceae (Poirel et al., 2017, Journal of Clinical Microbiology). Therapeutic strategies targeting this region focus on overcoming resistance or inhibiting the modification enzymes to restore antibiotic susceptibility (MacNair et al., 2018, Nature Communications).

Other names

pEtN-modified lipid APhosphoethanolamine-modified lipopolysaccharideMCR-modified lipid AColistin-resistant lipid ALipid A-pEtN

Cationic displacement of membrane-stabilizing divalent ions followed by binding to the lipid A moiety, leading to outer membrane disruption and cell death (Landman et al., 2008, Clinical Microbiology Reviews; Poirel et al., 2017, Journal of Clinical Microbiology).