Low biological activity of Helicobacter pylori lipopolysaccharide

Lipopolysaccharide of Helicobacter pylori was tested for its mitogenicity and for its ability to stimulate cytokine release in human peripheral blood mononuclear cells (PBMC) of healthy and H. pylori-infected blood donors. Mitogenicity in PBMC induced by H. pylori LPS was similar to that induced by Campylobacter jejuni lipopolysaccharide, but lower than that induced by Escherichia coli lipopolysaccharide in the H. pylori negative blood donor group. Furthermore, H. pylori LPS was able to induce tumour necrosis factor (TNF) interleukin 1 (IL-1) and interleukin 6 (IL-6) secretion of PBMC. Compared with the ability of C. jejuni and E. coli lipopolysaccharides to stimulate cytokine release, H. pylori lipopolysaccharide induced a significantly lower TNF and IL-1 secretion of PBMC than the other tested bacterial lipopolysaccharides. Similar amounts of IL-6 release were obtained by stimulation of PBMC with H. pylori and C. jejuni lipopolysaccharides, whereas a higher IL-6 release was measured by stimulation with E. coli lipopolysaccharide. The results of this study suggest that H. pylori lipopolysaccharide has a lower immunological activity than lipopolysaccharides of other intestinal bacteria. This is probably due to its unusual acylation and phosphorylation pattern of lipid A.

Section: Discussionmentioning

confidence: 56%

“…This might influence the biological activity of the LPS. Recently, in comparison to Salmonella enterica, a low biological activity of H. pylori LPS was demonstrated in mice [17].…”

Section: Introductionmentioning

confidence: 99%

Immunological activity of lipopolysaccharide of Helicobacter pylori on human peripheral mononuclear blood cells in comparison to lipopolysaccharides of other intestinal bacteria

Birkholz¹

1993

“…Based on the unusual fatty acid substitution in H, pylon' lipid A and the underphosphorylation of the lipid A backbone, we tested the hypothesis that H. pylori LPS should possess lower activities in classical endotoxic test systems. Supporting the hypothesis, the pyrogenicity and mitogenicity of H. pylon' LPS were lOOO-fold lower, the lethal toxicity in mice of H. pylon' LPS was 500-fold lower, compared with Salmonellu LPS[21]. Birkholz et al[22] found that TNF-a, IL-1 and IL-6 secretion by human mononuclear cells induced by H. pylon' LPS was significantly lower than that induced by E. coli LPS.…”

mentioning

confidence: 92%

Cell surface characteristics of Helicobacter pylori

Moran

1995

Helicobacter pylori is an important gastroduodenal pathogen of humans. Immunological and structural studies have been performed on the phospholipids, lipopolysaccharides (LPS) and some surface proteins of H. pylori strains. H. pylori LPS has, in general, low immunological activity and this property may aid the survival of this chronic infection. Nevertheless, H. pylori LPS has been found to influence the quality of gastric mucin and to stimulate pepsinogen secretion, thereby contributing to gastric disease. A number of putative adhesins of the bacterium have been described. This multiplicity of adhesins may reflect that H. pylori adherence is a multi-step process involving different interactions, and that different adhesins may mediate adherence to various sites in gastric tissue.

“…Pyrogenicity of LPS was tested in chinchilla rabbits which were bred, reared, and maintained in a conventional environment as described previously [21]. The pyrogen assay was performed according to the European Pharmacopoeia [22] using rabbits weighing 3.3-4 kg in groups of six.…”

Section: Pyrogenicity Assaymentioning

confidence: 99%

Biological and serological characterization of Campylobacter jejuni lipopolysaccharides with deviating core and lipid A structures

Moran

1995

Lipopolysaccharides from Campylobacter jejuni were tested for their ability to induce toxic lethality in galactosamine-sensitized mice, pyrogenicity in rabbits and tumour necrosis factor (TNF) secretion from mouse peritoneal macrophages. Compared with those of Salmonella LPS, lethal toxicity was 50% lower, pyrogenicity was 30- to 50-fold lower, and ability to induce TNF was 100-fold lower. C. jejuni LPS and lipid A exhibited higher phase-transition temperatures than those of Salmonella preparations, and thus the former have lower fluidity at 37 degrees C. This lower fluidity of acyl chains may influence the biological activities of C. jejuni LPS, but acyl chain characteristics and diaminoglucose replacing glucosamine in the hydrophilic lipid A backbone may also influence the supramolecular structure of lipid A, thereby affecting biological activities. Although diaminoglucose is present in the backbone of C. jejuni lipid A, antigenically the latter resembled classical lipid A of the Enterobacteriaceae when tested with anti-lipid A antibodies. Chemical investigations suggested the presence of glucuronic acid in an acid labile linkage in the inner core region, thus producing a structurally unusual region in C. jejuni LPS.