Structural Relationships and Sialylation among Meningococcal L1, L8, and L3,7 Lipooligosaccharide Serotypes

Eighteen of 34 endemic meningococcal case strains were of the L8 lipooligosaccharide (LOS) type; four of these were both L3 and L7 (L3,7), and seven were L1. L1 structures arose by alternative terminal Gal substitutions of lactosyl diheptoside L8 structures, as determined by electrospray ionization and other mass spectrometric techniques, and enzymatic and chemical degradations (Structures L1 and L1a).(NeuNAcα2)→Galα1→4Galβ1→4Glcβ1→4Hepα1→(Kdo)2 ↑ GlcNAc(OAc)α1→2Hep3←(PEA) STRUCTURE L1Galβ1→4Glcβ1→4Hepα1→(Kdo)2 ↑Galα1→4GlcNAc(OAc)α1→2Hep3←(PEA) STRUCTURE L1aThe more abundant molecule, designated L1, had a trihexose globosyl α chain; the less abundant one, designated L1a, had a β-lactosyl α chain and a parallel α-lactosaminyl γ chain. A P k globoside (Galα1→4Galβ1→4 Glc-R) monoclonal antibody bound 9/10 L1 strains, but a P1 globoside (Galα1→4Galβ1→4GlcNAc-R) mAb bound none of them. α-Galactosidase caused loss of both L1 structures and creation of L8 structures; β-galactosidase caused loss of the L8 determinant. The L1/P k glycose was partially sialylated. Some LOS also had unsubstituted basal β-GlcNAc additions. These structural relationships explain co-expression of L8, L1, and L3,7 serotypes.