Lipopolysaccharides (LPS) endotoxins of the outer leaflet of Gram-negative bacteria have a variety of biological effects on numerous types of mammalian cells. B lymphocytes are activated by LPSs to differentiate into antibody secreting plasma cells in the absence of specific antigens . The macrophages activated by LPSs produce a variety of cytokines (TNF, IL-1, IL-6), procoagulant activators, eicosanoids, reactive oxygen and nitrogen intermediates. LPS may also activate T cells. However, the majority of the effects of LPSs on T cells seem to be derived indirectly from the interaction between T cells and LPS-stimulated macrophages and from the mediators released from the LPS-activated accessory cells and cytokine-activated T cells . A role of an interaction between macrophage CD14 antigen, a cellular binding site for LPSs, with IL-2 produced by T cells, in the activation of human monocytes has been reported . Like the cell envelopes of other Gram-negative bacteria, that of Helicobacter pylori contains LPS. However, H. pylori LPS shows significantly lower mitogenicity, pyrogenicity, toxicity  and activity in mediation of macrophage activation  than LPSs of enterobacterial bacteria do. On the basis of structural study, the lower immunological activity of H. pylori LPS has been explained by underphosphorylation and underacylation of its lipid A moiety compared with those from enterobacterial LPS . Considering the chronic nature of H. pylori infections it was suggested that H. pylori LPS evolved its present structure as a consequence of adaptation to chronic infection of the gastric mucosa. Perhaps the evolution has led to co-expression of common complex carbohydrates, such as Lewis X and Lewis Y determinants, which are present on the LPSs of most H. pylori strains and in human cell surface glycoconjugates of blood cells and gastric mucosa [7,8]. Based on this molecular mimicry Appelmelk et al.  speculate on the role of autoimmune mechanisms in H. pylori-associated type B gastritis. Recently, it has been shown that an intravenous administration of a purified LPS from H. pylori induced in rats an increased vascular permeability in cardiac, renal, hepatic, pulmonary and intestinal tissues, which could be prevented by the selectively inducible nitric oxide synthase inhibitor [10,11]. In contrast, H. pylori LPS-induced gastric mucosal inflammatory response in rats was enhanced by aspirin . During natural H. pylori infections in humans, antibodies (mainly of IgG class) to polysaccharide chains of LPSs of those bacteria are produced [13,14]. However, the antigenicity of the polysaccharide varied, depending on the strain. It has been found that smooth H. pylori strains isolated from the tumors of patients with gastric cancer showed significantly lower antigenicity than smooth strains derived from patients with chronic gastritis and gastric and duodenal ulcers . If anti-H. pylori LPS IgG and IgA antibodies are produced in H. pylori-infected subjects one may speculate that an activation of T lymphocytes or at least of T helper cells by bacterial LPS is very likely. In this study, we examined the proliferative response to H. pylori LPS of peripheral blood mononuclear leukocytes (PBML) from children and young adolescents with chronic dyspepsia, seropositive for anti-H. pylori IgG, in cultures with or without IL-2 as a growth factor of T cells. All patients were examined by endoscopy and a type B gastritis in gastric mucosa was evaluated. Gastric mucosal biopsy specimens were used for detecting bacterial urease in a rapid urease test (RUT) and Helicobacter-like organisms (HLO) in histological sections. The results suggest that H. pylori LPS may influence an outcome of H. pylori infection by activation of T cells. Probably, activated lymphocytes may, at least in some patients, facilitate a control of bacterial growth and diminish inflammation in gastric mucosa by releasing cytokines, possibly of Th2 type.