An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection

Colonize, evade, flourish

“…The Fut protein ruler mechanism is illustrated by length of protein corresponding to length of O-chain sugar that is fucosylated. 38 The completed O-chain containing Lewis antigens (patterned fucose residues linked to GlcNAc and galactose sugars) is translocated to the periplasmic face of the inner membrane by wzk. Finally, it is removed from the UndPP carrier and transferred onto the lipid A/core by waaL, generating a mature LPS species.…”

“…FutA and FutB are characterized by C-terminal heptad-repeat regions of variable length that allow homo-and heterodimerization. Further, Nilsson et al 38 presented a molecular addition of fucose to carbon 3 of the GlcNAc sugar, instead of carbon 4. In H. pylori, Le x and Le y antigens are prevalent relative to other Le structures, found in 80-90% of strains across the world; however, a and b structures have been detected at low frequencies in both Asian and European isolates.…”

“…In explanation, they show that one heptad-repeat corresponds to one Gal-GlcNAc backbone unit in the glycan chain, such that the location of the active site and recipient sugar residue are finely controlled. 38 5 In addition, the fucosyltransferase and β(1,3) GalT genes are subject to phase variation, or random switching on and off of expression during the lifetime of a given bacterial cell. 34,39 This leads to an expansive diversity of possible Le antigen patterns across a population of H. pylori cells during the course of infection.…”

A Double-Edged Sword: Roles of Helicobacter Pylori in Gastric Carcinoma

“…pylori has evolved means to structurally alter its surface characteristics to evade innate and adaptive immune responses (Nilsson et al, 2006). H. pylori expresses mimicry of some ABO blood group antigens (Moran et al, 2010).…”

“…H. pylori LPS is of underacylation and underphosphorylation and has significantly lower endotoxic and immuno-activities, which may lead to the infection chronicity (Moran et al, 2010). H. pylori produces LPS O-antigen units that can be posttranslationally fucosylated to generate Lewis antigens, which are also found on human GECs, and this molecular mimicry induces autoreactive antibodies (Nilsson et al, 2006). Circulating anti-Lewis antibody is detected in the sera of GC patients but not in H. pylori-negative control subjects (Hynes et al, 2005).…”