Lipopolysaccharide structures of Helicobacter pylori genomic strains 26695 and J99, mouse model H. pylori Sydney strain, H. pylori P466 carrying sialyl Lewis X, and H. pylori UA915 expressing Lewis B

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Abstract
This study describes the molecular makeup of the cell‐wall lipopolysaccharides (LPSs) (O‐chain polysaccharide→core oligosaccharide→lipid A) from five Helicobacter pylori strains: H. pylori 26695 and J99, the complete genome sequences of which have been published, the established mouse model Sydney strain (SS1), and the symptomatic strains P466 and UA915. All chemical and serological experiments were performed on the intact LPSs. H. pylori 26695 and SS1 possessed either a low‐Mr semi‐rough‐form LPS carrying mostly a single Ley type‐2 blood‐group determinant in the O‐chain region covalently attached to the core oligosaccharide or a high‐Mr smooth‐form LPS, as did strain J99, with an elongated partially fucosylated type‐2 N‐acetyllactosamine (polyLacNAc) O‐chain polymer, terminated mainly by a Lex blood‐group determinant, connected to the core oligosaccharide. In the midst of semi‐rough‐form LPS glycoforms, H. pylori 26695 and SS1 also expressed in the O‐chain region a difucosylated antigen, α‐l‐Fucp(1–3)‐α‐l‐Fucp(1–4)‐β‐d‐GlcpNAc, and the cancer‐cell‐related type‐1 or type‐2 linear B‐blood‐group antigen, α‐d‐Galp(1–3)‐β‐d‐Galp(1–3 or 4)‐β‐d‐GlcpNAc. The LPS of H. pylori strain P466 carried the cancer‐associated type‐2 sialyl Lex blood‐group antigen, and the LPS from strain UA915 expressed a type‐1 Leb blood‐group unit. These findings should aid investigations that focus on identifying and characterizing genes responsible for LPS biosynthesis in genomic strains 26695 and J99, and in understanding the role of H. pylori LPS in animal model studies. The LPSs from the H. pylori strains studied to date were grouped into specific glycotype families.

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