title: Lipid A in Helicobacter pylori.
abstract: Free lipid A of Helicobacter pylori was characterized with regard to chemical composition, reactivity with anti-lipid A antibodies, and activity in a Limulus lysate assay. The predominant fatty acids of H. pylori lipid A were 3-OH-18:0, 18:0, 3-OH-16:0, 16:0, and 14:0. Hexosamine was present in amounts similar to those in Campylobacter jejuni or Salmonella typhimurium lipid A. The lipopolysaccharide of H. pylori contained 2-keto-3-deoxyoctonic acid, a common constituent of enterobacterial and C. jejuni lipopolysaccharides. In the enzyme-linked immunosorbent assay, the doses of lipid A required to inhibit anti-lipid A by 50% (EI50 values) by absorption of the immune (rabbit) serum were 7.9, 1.2, and 1.4 micrograms of O-deacylated lipid A's from H. pylori, C. jejuni, and S. typhimurium per ml, respectively. The lower reactivity of H. pylori lipid A compared with those of the other two lipid A preparations (as shown by the higher EI50 value) was underscored by the use of a murine monoclonal anti-lipid A antibody in the inhibition assay. An EI50 value was not obtained at the concentrations tested for H. pylori lipid A; the corresponding figures for C. jejuni and S. typhimurium lipid A's were 13 and 14 micrograms/ml, respectively. No inhibition was obtained with H. pylori lipopolysaccharide, which showed a low-molecular-weight profile on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The activity of H. pylori lipid A in the Limulus assay was approximately 71 and 650 times lower than those of C. jejuni and S. typhimurium lipid A's, respectively. These findings suggest that lipid A is an integral part of the outer cell wall of H. pylori. The lower reactivity of H. pylori lipid A with anti-lipid A antibodies and in the Limulus assay compared with that of C. jejuni or S. typhimurium lipid A may be explained by a different composition of the fatty acids, especially the 3-hydroxy fatty acids, and a possible deviating phosphorylation pattern.
authors.affiliation: Department of Clinical Bacteriology, University of Göteborg, Sweden.
authors.forename: I
authors.initials: I
authors.lastname: Mattsby-Baltzer
authors.forename: Z
authors.initials: Z
authors.lastname: Mielniczuk
authors.forename: L
authors.initials: L
authors.lastname: Larsson
authors.forename: K
authors.initials: K
authors.lastname: Lindgren
authors.forename: S
authors.initials: S
authors.lastname: Goodwin
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D016480:Helicobacter pylori / Q000737:chemistry* / Q000472:pathogenicity; D008033:Limulus Test; D008050:Lipid A / Q000032:analysis* / Q000276:immunology / Q000633:toxicity; D008070:Lipopolysaccharides / Q000032:analysis / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D011817:Rabbits
chemical_list: D000911:Antibodies, Monoclonal; D008050:Lipid A; D008070:Lipopolysaccharides