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Escherichia coli surface polysaccharides, primarily comprising lipopolysaccharides (LPS) and capsular polysaccharides (CPS or K-antigens), are complex carbohydrate structures that coat the bacterial cell surface. These molecules are vital for the bacterium's survival, serving as a protective barrier against environmental stressors and host immune mechanisms, such as the complement system and antimicrobial peptides (Raetz & Whitfield, 2002; Whitfield, 2006). LPS, a hallmark of Gram-negative bacteria, consists of lipid A, a core oligosaccharide, and the O-antigen, the latter of which is highly variable and used for serotyping (Stenutz et al., 2006). These polysaccharides also act as primary receptors for many bacteriophages, which recognize specific sugar motifs to initiate infection (Bertozzi Silva et al., 2016). In clinical medicine, LPS is a major driver of Gram-negative sepsis, as its lipid A component is recognized by the host's TLR4/MD2 complex, triggering a massive pro-inflammatory cytokine release (Park & Lee, 2013). Therapeutic strategies targeting these structures include the use of polymyxin antibiotics, which bind to LPS to disrupt the outer membrane, and the development of serotype-specific vaccines and monoclonal antibodies designed to enhance bacterial clearance or neutralize endotoxin activity (Cross, 2014; Poirel et al., 2017).
Polymyxins bind to the lipid A moiety of lipopolysaccharides, displacing stabilizing divalent cations and disrupting the outer membrane integrity. Monoclonal antibodies and vaccines target specific O or K antigens to facilitate opsonophagocytosis and neutralize endotoxin-mediated inflammatory signaling.
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