Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.5 (urease)
 7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inflammatory lesions associated with Helicobacter pylori gastritis and duodenitis contain large numbers of mononuclear cells. The close proximity of H. pylori to gastric mucosa suggests that the organism interacts with mononuclear cells, thereby modulating the inflammatory response. To investigate the role of monocytes/macrophages in this response, we examined the effect of whole H. pylori bacteria, H. pylori surface proteins, and H. pylori lipopolysaccharide (LPS) on purified human monocytes. Whole H. pylori and the extracted LPS induced expression of the monocyte surface antigen HLA-DR and interleukin-2 receptors, production of the inflammatory cytokines interleukin 1 and tumor necrosis factor (peptide and messenger RNA), and secretion of the reactive oxygen intermediate superoxide anion. Since H. pylori in vivo does not invade mucosal tissue, we determined whether soluble constituents of the bacteria could activate monocytes. Soluble H. pylori surface proteins, which are enriched for urease and do not contain LPS, stimulated phenotypic, transcriptional, and functional changes consistent with highly activated monocytes. These findings indicate that H. pylori is capable of activating human monocytes by an LPS-independent as well as an LPS-dependent mechanism. H. pylori activation of resident lamina propria macrophages and monocytes trafficking through the mucosa, leading to the secretion of increased amounts of inflammatory cytokines and reactive oxygen intermediates, could play an important role in mediating the inflammatory response associated with H. pylori gastritis and duodenitis.
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PMID:Soluble surface proteins from Helicobacter pylori activate monocytes/macrophages by lipopolysaccharide-independent mechanism. 184 39

We isolated lymphocytes from chronically inflamed gastric mucosa. We analysed the expression of IL-2 receptors (CD25), transferin receptors (CD71) and HLA-DR molecules on T lymphocytes by flow cytometric analysis in 16 patients with urease-positive and in 7 patients with urease-negative chronic gastritis. In G0, G1 and G2 histological type (Sydney classification) of gastritis the number of lymphocytes obtained from the gastric mucosa biopsies was too low for the flow cytometric analysis. However, in G3 histological type of chronic gastritis we obtained enough cells for the flow cytometric analysis in 75%. We demonstrated a significant increase in HLA-DR expression on CD8 cells from patients with urease-positive gastritis compared to urease-negative gastritis. We also observed a statistically non-significant increase in HLA-DR expression on CD3 cells, and in CD71 expression on both CD3 and CD8 cells in urease-positive gastritis. However, no difference in CD25 expression was found between the two types of gastritis.
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PMID:HLA-DR expression on CD8 lymphocytes from gastric mucosa in urease-positive and urease-negative gastritis. 777 47

Ten patients with Helicobacter pylori-associated chronic gastritis were given combination therapy for 6 weeks with a bismuth subnitrate-containing compound and bacampicillin. The eradication rate was 40% 6 weeks after the end of treatment. Two patients remained H. pylori-negative at long-term follow-up after 6 and 17 months; that is, H. pylori was only eradicated in 20% of the patients after long-term observation. By dot blot and immunoblotting both urease and an urease-associated heat shock protein (HSP62) were found to be specific and constant immunodominant H. pylori antigens. The immunohistologic pattern showed induced expression of HLA-DR and HSP62, but not of ICAM-1, in all but two biopsy specimens of gastric epithelial cells. This study suggests i) that long-term observation is important when evaluating the efficacy of anti-H. pylori therapy; ii) that the immune defense mechanisms in the gastric mucosa differ from those in inflammatory conditions affecting other organs, where ICAM-1 and HLA-DR seem to be governed by a common regulator; and iii) that the immunopathologic effects of H. pylori may be caused by autologous and/or bacterial HSPs, which act as triggering factors in the development and persistence of the chronic inflammation in the gastric mucosa.
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PMID:Local and systemic immune response in Helicobacter pylori-associated chronic gastritis before and after treatment. 790 61

The ability of 23 different strains of Helicobacter pylori to induce proliferative response of human peripheral blood mononuclear cells (PBMC) was investigated. All tested strains stimulated the DNA synthesis of PBMC from both healthy and H. pylori infected blood donors, but with lower stimulation of PBMC of infected donors. Using different bacterial antigen preparations, such as crude membranes, cytoplasmic proteins, and urease, a significantly lower induction of the proliferative response of PBMC from H. pylori infected than from healthy blood donors could also be demonstrated. In contrast to this result the reaction to phytohemagglutinin and purified protein derivative of tuberculin was similar in both groups. The stimulation pathway was interleukin 2 (IL-2) dependent as proved by inhibition of the proliferative response with an alpha-IL-2-receptor antibody. Using an antibody against HLA-DR the lymphoproliferation could also be blocked showing the importance of the major histocompatibility class II (MHCII) complex. Only coincubation of T cells with monocytes plus antigen or with antigen-preincubated monocytes led to a proliferative response showing the necessity of antigen-presenting cells. At least a part of the lymphoproliferative response is MHCII restricted as could be shown with H. pylori specific T-cell lines. These results and the kinetics of the proliferative response with a maximum at day 7 suggest that the proliferative response of human PBMC was mainly induced by antigens than by a mitogen.
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PMID:Stimulatory effects of Helicobacter pylori on human peripheral blood mononuclear cells of H. pylori infected patients and healthy blood donors. 828 Sep 39