Helicobacter pylori causes a persistent infection in the human stomach, which can result in chronic gastritis and peptic ulcer disease. Despite an intensive proinflammatory response, the immune system is not able to clear the organism. However, the immune escape mechanisms of this common bacterium are not well understood. We investigated the interaction between H. pylori and human dendritic cells. Dendritic cells (DCs) are potent antigen-presenting cells and important mediators between the innate and acquired immune system. Stimulation of DCs with different concentrations of H. pylori for 8, 24, 48, and 72 h resulted in dose-dependent interleukin-6 (IL-6), IL-8, IL-10 and IL-12 production. Lipopolysaccharide (LPS) from Escherichia coli, a known DC maturation agent, was used as a positive control. The cytokine release after stimulation with LPS was comparable to that induced by H. pylori except for IL-12. After LPS stimulation IL-12 was only moderately released compared to the large amounts of IL-12 induced by H. pylori. We further investigated the potential of H. pylori to induce maturation of DCs. Fluorescence-activated cell sorting analysis of cell surface expression of maturation marker molecules such as CD80, CD83, CD86, and HLA-DR revealed equal upregulation after stimulation with H. pylori or LPS. We found no significant differences between H. pylori seropositive and seronegative donors of DCs with regard to cytokine release and upregulation of surface molecules. These data clearly demonstrate that H. pylori induces a strong activation and maturation of human immature DCs.Helicobacter pylori is a gastric pathogenic gram-negative bacterium that colonizes the gastric mucus layer but does not invade the mucosal epithelium. This bacterial colonization leads to a cellular infiltrate of polymorphonuclear leukocytes, an acute immune response, followed by the migration of macrophages, lymphocytes, and plasma cells in the gastric mucosa, resulting in chronic gastritis. This chronic inflammation does not necessarily produce symptoms but does increase the risk of developing peptic ulcer disease, adenocarcinoma of the distal stomach (antrum and fundus), and primary non-Hodgkin's lymphoma of the stomach (MALTomas) (8,42,43).Although H. pylori induces an immune response involving both the innate and the acquired immune systems, the host is unable to clear the organism from the mucosa, resulting in lifelong infection. This inability to eliminate the bacterium may be due to immune-evasive strategies. Possible mechanisms were investigated, with emphasis on the acquired immune response. Several studies have shown inhibitory effects of H. pylori on cell proliferation (11, 24-26, 60), and the induction of H. pylori-specific regulatory T cells that actively suppress T-cell response have been described (31).Recent studies have investigated possible impairment of antigen presentation. VacA, an H. pylori virulence factor, was reported to interfere with proteolytic processing of tetanus toxoid and was shown to inhibit the Ii-depen...
