Lipid A is the reason lipopolysaccharide (LPS) in Gram-negative bacterial cell walls acts as an endotoxin.

Option Analysis

Lipid A anchors LPS in the outer membrane and contains the toxic moiety—a phosphorylated glucosamine disaccharide with multiple fatty acid chains. It triggers severe immune responses like cytokine storms and septic shock upon release, making LPS an endotoxin.

Core polysaccharide (or core oligosaccharide) links Lipid A to the O side chain, containing sugars like KDO, heptose, and hexoses for structural stability, but lacks toxicity.

O side chain (O-antigen) is a repeating polysaccharide on the outer surface providing serological specificity and immune evasion, with no inherent endotoxic activity.​

Integral proteins embed in the membrane for transport and structure but are unrelated to LPS toxicity or endotoxin properties.​

Lipopolysaccharide present in Gram negative bacterial cell wall is considered as an endotoxin because of Lipid A, the conserved lipid anchor driving immune hyperactivation during infections. LPS forms the outer membrane barrier, but Lipid A’s release causes sepsis, distinguishing endotoxins from exotoxins.

LPS Structure and Toxicity

LPS comprises Lipid A (toxic core), core polysaccharide (inner/outer regions with KDO/heptose), and O side chain (variable antigen). Lipid A, with its β-1,6-linked glucosamines, four to seven acyl chains, and phosphates, binds TLR4/MD2/CD14, unleashing TNF-α, IL-1, and nitric oxide.​

Component Roles

Core stabilizes LPS; O-antigen aids phage resistance and serotyping; proteins handle unrelated functions. Only Lipid A elicits endotoxicity, varying slightly by species but universally potent at pg/mL levels.

This confirms Lipid A as why lipopolysaccharide present in Gram negative bacterial cell wall is considered as an endotoxin because of its pyrogenic potency in exams.