Salmonella enterica serovar Typhi lipopolysaccharide (S. Typhi LPS)

Salmonella enterica serovar Typhi lipopolysaccharide (LPS) is a major glycolipid component of the outer membrane of S. Typhi, the causative agent of human typhoid fever. LPS consists of lipid A (endotoxin), a core oligosaccharide, and a variable O-antigen polysaccharide. It plays a crucial role in resistance to host immune responses, particularly by providing serum resistance, modulating phagocytosis, and mediating bacterial internalization into epithelial cells. The structure of the LPS, including the length and composition of its O-antigen and outer core, is critical for its function in immune evasion and pathogenesis. Alterations in LPS biosynthesis impact the ability of S. Typhi to infect host cells and survive in hostile environments, including in the presence of antimicrobials. LPS and its biosynthetic machinery, such as the glucosyltransferase RfaJ, are studied as potential therapeutic targets, especially given the rising antibiotic resistance in S. Typhi[1][2][3].

Other names

S. Typhi LPSSalmonella Typhi LPSTyphoid bacillus lipopolysaccharide

Disruption of LPS biosynthesis (e.g., inhibition of glycosyltransferase RfaJ impairs LPS assembly and function)[2] Direct binding/disruption of LPS (e.g., cationic peptides and antibiotics like colistin interact with the outer LPS structure, altering membrane integrity leading to bacterial death)[1]