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

Abstract

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.

Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

“…H. pylori LPS is able to induce toxic lethality in animal models 62 and the secretion of cytokines by human monocytes. 63,64 However, this induction is weaker than that of other tested bacterial LPS. This lower immunological activity of H. pylori LPS is probably a result of its unusual acylation and phosphorylation pattern of lipid A.…”

“…This lower immunological activity of H. pylori LPS is probably a result of its unusual acylation and phosphorylation pattern of lipid A. 63 H. pylori LPS may have an important role in autoimmune-mediated damage in the gastric mucosa. The structure of the LPS O-specific chain in different H. pylori strains may mimic Lewis blood group antigens in structure.…”

Ecabet sodium inhibitsHelicobacter pylorilipopolysaccharide-induced activation of NADPH oxidase 1 or apoptosis of guinea pig gastric mucosal cells

“…Because endotoxic activity of H. pylori LPS is much lower than LPS from the other enterobacteria (4,26,30), H. pylori LPS is not generally considered as a crucial virulence. On the other hand, guinea pig gastric pit cells, chief cells (46), and enterochromaffin-like cells (20) are highly responsive to H. pylori LPS.…”

“…The chemical structure of H. pylori LPS is different from those of other enterobacterial LPSs (5,9,25), and its endotoxic properties are very low compared with other enterobacterial preparations (4,26,30). On the other hand, it was reported that H. felis caused severe atrophic gastritis in C3H/He mice, whereas C3H/HeJ mice with a mutated Toll-like receptor 4 (TLR4) gene showed heavy colonization but minimal atrophic gastritis with much less macrophage infiltration (34).…”

Pro- and Antiphlogistic Concentration of Cytokines in Rats’ Serum after Long-Term Administration of Omeprazole and the Simultaneous Injection of Multiprobiotics and Omeprazole

“…Відомо, що ліпополісахариди, які є головними компонентами зовнішньої мембрани аеробних грам-негативних бактерій E. coli (ендотоксини), у 1000 разів сильніше впливають на виділення про-запальних цитокінів, ніж ліпополісахариди H. pylori [13]. Експериментальні дослідження також показа-ли, що бактеріальні ліпополісахариди порушують процеси гоєння в слизовій оболонці шлунка через зменшення кровотоку в слизовій оболонці шлунка, збільшену експресію та вивільнення про-запальних цитокінів ІЛ-1β та ФНП-α, дисбаланс між про-та анти-апоптичними членами родини Bcl-2 [15].…”