Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection causes chronic gastritis that may progress to peptic ulcers or gastric adenocarcinoma and thereby cause major world-wide health problems. Previous studies have shown that CD4+ T cells are important in the immune response to H. pylori in humans, but the role of CD8+ T cells is less clear. In order to study the CD8+ T cell response to H. pylori in greater detail, we have evaluated efficient conditions for activation of CD8+ T cells in vitro. We show that H. pylori-reactive CD8+ T cells can be activated most efficiently by B cells or dendritic cells pulsed with H. pylori antigens. We further show that the majority of CD8+ T cells in H. pylori-infected gastric mucosa are memory cells, and that memory CD8+ T cells sorted from peripheral blood of H. pylori-infected individuals respond 15-fold more to H. pylori urease compared to memory cells from uninfected subjects. We conclude that CD8+ T cells do participate in the immune response to H. pylori, and this may have implications for the development of more severe disease outcomes in H. pylori-infected subjects.
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PMID:B cells pulsed with Helicobacter pylori antigen efficiently activate memory CD8+ T cells from H. pylori-infected individuals. 1632 87

Helicobacter pylori is one of the most common bacterial infections worldwide. It is associated with chronic gastritis, peptic ulcer disease and constitutes a major risk factor for gastric adenocarcinoma and lymphoma. The aim of this study was to evaluate the specific serologic immunoglobulin G (IgG) response to whole cells proteins, CagA and urease antigens of Helicobacter pylori in a Venezuelan population. We evaluated 66 patients from the Hospital Universitario de Caracas, attending in the gastroscopy service. H. pylori infection was detected by culture and rapid urease test. IgG antibodies against, CagA and ureases were tested by enzyme-linked immunosorbent assay method using highly purified recombinant antigens. We demonstrated the presence of H. pylori in 48/66 (72.7%), by culture and rapid urease test. We found a seroprevalence of 45 (68%) to whole cells, 34/66 (51%) to CagA and 18/66 (27%) to urease. The positive rates of CagA antibodies in patients with gastric ulcer, gastric cancer and chronic gastritis were 87.8%, 77.7% y 40.8% respectively. The serum antibodies anti-CagA were similar between peptic ulcer disease and gastric cancer patients.
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PMID:[Importance of IgG anti-CagA antibodies of Helicobacter pylori in Venezuelan patients with gastric diseases]. 1635 43

Helicobacter pylori, a gram-negative, microaerophilic, motile, spiral-shaped bacterium, has been established as the etiologic agent of gastritis and peptic ulcers and is a major risk factor for gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (MALT). The ability of H. pylori to cause this spectrum of diseases depends on host, bacterial, and environmental factors. Bacterial factors critical for H. pylori colonization of the gastric mucosa include urease, flagella, adhesins, and delta-glutamyltranspeptidase. Lipopolysaccharide, urease, and vacuolating cytotoxin are among the factors that allow H. pylori to persist for decades and invoke an intense inflammatory response, leading to damaged host cells. Genes in the cag pathogenicity island also contribute to the inflammatory response by initiating a signal transduction cascade, resulting in interleukin-8 production. Proinflammatory cytokines and a Th-1 cytokine response further exacerbates the inflammation. Products of the enzymes nitric oxide synthase (iNOS) and cyclooxygenase may perturb the balance between gastric epithelial cell apoptosis (ulcer formation) and proliferation (cancer). The host Th-1 response and antibodies directed against H. pylori do not eliminate the organism, which presents challenges to vaccine development. Vaccines that include urease have shown some promise, but improved adjuvants and animal models should hasten progress in vaccine research. H. pylori is the most genetically diverse organism known, and the panmictic population structure may contribute to the varying ranges of disease severity produced by different strains. The complete genome sequence of two strains of H. pylori has propelled this field forward, and numerous groups are now using genomic, proteomic, and mutagenetic approaches to identify new virulence genes. Discovered only in 1982, H. pylori is now among the most intensely investigated organisms. This review summarizes recent progress in this rapidly moving field.
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PMID:Pathogenesis of Helicobacter pylori infection. 1702 12

Both Helicobacter pylori and "Candidatus Helicobacter heilmannii" infections are associated with peptic ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. However, good animal models of H. pylori clinical diseases are rare. In this study, we aimed to establish an animal model of "Candidatus Helicobacter heilmannii" gastric MALT lymphoma. We used a urease-positive gastric mucosal and mucus homogenate from a cynomolgus monkey maintained in C57BL/6 mouse stomachs. The bacterium in the homogenate was identified as "Candidatus Helicobacter heilmannii" based on a DNA sequence analysis of the 16S rRNA and urease genes. Mucosal and mucus homogenates were used to inoculate C57BL/6 mice, which were then examined for 24 months. We observed a gradual increase in the surface area of protrusive lesions in almost all infected C57BL/6 mouse fundic stomachs 6 months after infection. Light microscopic observations revealed an accumulation of B lymphocytes along with destruction of glandular elements and the presence of lymphoepithelial lesions consistent with low-grade MALT lymphomas. Electron microscopic observation revealed numerous "Candidatus Helicobacter heilmannii" bacilli in the fundic glandular lumen, the intracellular canaliculi, and the cytoplasm of intact cells, as well as damaged parietal cells. In conclusion, "Candidatus Helicobacter heilmannii" induced gastric MALT lymphomas in almost 100% of infected C57BL/6 mice after a 6-month period associated with the destruction of parietal cells.
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PMID:"Candidatus Helicobacter heilmannii" from a cynomolgus monkey induces gastric mucosa-associated lymphoid tissue lymphomas in C57BL/6 mice. 1719 7

Helicobacter pylori, a Gram-negative flagellate bacterium that infects the stomach of more than half of the global population, is regarded as the leading cause of chronic gastritis, peptic ulcer disease, and even gastric adenocarcinoma in some individuals. Although the bacterium induces strong humoral and cellular immune responses, it can persist in the host for decades. It has several virulence factors, some of them having vaccine potential as judged by immunoproteomic analysis. A few vaccination studies involving a small number of infected or uninfected humans with various H. pylori formulations such as the recombinant urease, killed whole cells, and live Salmonella vectors presenting the subunit antigens have not provided satisfactory results. One trial that used the recombinant H. pylori urease coadministered with native Escherichia coli enterotoxin (LT) demonstrated a reduction of H. pylori load in infected participants. Although extensive studies in the mouse model have demonstrated the feasibility of both therapeutic and prophylactic immunizations, the mechanism of vaccine-induced protection is poorly understood as several factors such as immunoglobulin and various cytokines do not contribute to protection. Transcriptome analyses in mice have indicated the role of nonclassical immune factors in vaccine-induced protection. The role of regulatory T cells in the persistence of H. pylori infection has also been suggested. A recently developed experimental H. pylori infection model in humans may be used for testing several new adjuvants and vaccine delivery systems that have been currently obtained. The use of vaccines with appropriate immunogens, routes of immunization, and adjuvants along with a better understanding of the mechanism of immune protection may provide more favorable results.
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PMID:The current status of Helicobacter pylori vaccines: a review. 1730 45

Helicobacter pylori infection is the most common cause of gastritis, gastric ulcer and adenocarcinoma. It has proven difficult to cure because of its capability to develop strains resistant to antibiotics. The effect of three strains of lactic acid bacteria (LAB) and bovine colostral preparations on the adhesion of H. pylori NCTC 11637 on gastric adenocarcinoma (AGS) cells and on the interleukin (IL)-8 production was studied. Before infection, H. pylori were pretreated with Lactobacillus plantarum MLBPL1, Lactobacillus rhamnosus GG, Lactococcus lactis, or with a colostral preparation with or without specific H. pylori antibodies. The relative number of H. pylori adhered on AGS cells was determined by urease test. IL-8 produced by the cells was studied by enzyme-linked immunosorbent assay. Colostral preparations with and without specific antibodies reduced the adhesion of H. pylori on AGS cells in a dose-dependent manner. Live LAB at a concentration of 10(10) CFU/ml reduced the adhesion by approximately 50% (P < 0.05). After the infection of AGS cells by H. pylori, the IL-8 level rose up to about 10-fold (5500 +/- 1600 pg/ml). Pretreatment of H. pylori with colostral preparations or high concentrations of LAB prevented this IL-8 rise. Similar effect was seen with live and heat-killed LAB, the live LAB being more effective. Heat-killed LAB at a concentration of 10(10) CFU/ml rose the IL-8 level of non-infected cells significantly. Suppression of IL-8 production by LAB or colostral products could have a suppressive effect on inflammation in Helicobacter infection.
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PMID:Effect of specific colostral antibodies and selected lactobacilli on the adhesion of Helicobacter pylori on AGS cells and the Helicobacter-induced IL-8 production. 1862 49

Chronic Helicobacter (H.) pylori infection is an etiological factor related to gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. The expression of bcl-2 protein significantly decreases as the grade of MALT lymphoma advances. The aim of this study was to evaluate bcl-2 expression in inflammatory cells in lamina propria in gastric biopsy samples collected from two groups of patients with chronic gastritis divided on the basis of the success or failure of H. pylori eradication. Sixty-five patients with chronic gastritis were divided into two groups of 45 and 20 patients according to their therapeutic response. The gastric mucosa samples were analyzed histologically in both groups of patients before and after standard therapy (for eradicated, after one therapeutic cycle; and for non-eradicated, after three therapeutic cycles) for H. pylori density, urease activity and bcl-2 expression. In the eradicated group of patients, H. pylori eradication was accompanied by significantly lower grades of bacterial colonization and lower urease activity in the corpus and antrum. Bcl-2 expression in inflammatory cells showed no statistically significant changes in either patient group at either location. There was no between-group difference in bcl-2 expression either. In conclusion, persistent long-lasting H. pylori infection is associated with higher grades of bacterial colonization and higher urease activity but not with bcl-2 expression in inflammatory cells.
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PMID:Influence of Helicobacter pylori infection persistence on bcl-2 expression in gastric mucosa inflammatory cells. 1917 59

The main conclusions drawn from the presentations related to Helicobacter pylori at Digestive Diseases Week 2008 are summarized. Several strains of H. pylori frequently infect the same patient, and consequently samples for culture should be obtained from the gastric antrum and body. The test-and-treat strategy in dyspepsia is as effective as empirical antisecretory therapy and is probably cheaper. The benefit of eradication therapy in patients with uninvestigated dyspepsia, although small, seems to be lasting. Eradication in the general population seems to reduce the development of dyspeptic symptoms in the long term and consequently could be cost-effective. The prevalence of H. pylori infection in peptic ulcer is decreasing and the frequency of idiopathic ulcers is increasing. Patients with H. pylori-negative bleeding ulcers have a high probability of hemorrhagic recurrence and should therefore receive maintenance antisecretory therapy. H. pylori eradication reduces the incidence of gastric adenocarcinoma, which could warrant a screening and treatment strategy for this infection in the general population in high risk areas. H. pylori infection should be eradicated in patients undergoing endoscopic mucosal resection for early gastric cancer. To prevent the development of gastric cancer, eradication therapy should be administered early, before gastric atrophy develops. H. pylori-negative and H. pylori-positive gastric lymphomas have an equally favorable prognosis. New diagnostic techniques have been developed: the ultra-rapid urease test, a simpler 14C-urea breath test, and an ELISA method for rapid bacterial susceptibility determination. In patients with gastrointestinal bleeding, the 13C-urea breath test performed immediately after emergency gastroscopy allows early diagnosis of infection. Eradication regimens with double doses of proton pump inhibitors are more effective than those with standard doses. "Sequential" therapy is more effective and cheaper than classical triple-drug therapy, although the superiority of administering therapy sequentially rather than concomitantly has not been established. In penicillin-allergic patients, a combination with levofloxacin and clarithromycin is a promising alternative in rescue therapy. Second-line rescue therapy with levofloxacin is effective and is also simpler and better tolerated than quadruple-drug therapy. The rate of quinolone resistance is increasing as a result of the widespread use of these antibiotics. Third-line treatment with levofloxacin is also a promising alternative. Even after the failure of three previous treatments, a fourth empirical rescue therapy (with levofloxacin or rifabutin) can be effective in more than half of patients. The annual recurrence rate of H. pylori infection is approximately 3% in developed countries and is higher than 10% in developing countries.
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PMID:[Helicobacter pylori-related diseases: dyspepsia, ulcer and gastric cancer]. 1943 62

This is a cross-sectional study on 140 gastric neoplasm subjects diagnosed by upper gastrointestinal endoscopy. The commonest site of cancer was the antrum of stomach (52.86%), followed by the antrum and body (32.86%) and only body region (12.14%). Histology revealed adenocarcinoma in all patients. The associations of Helicobacter pylori with gastric cancer were studied by rapid urease test, serology and histology by Giemsa stain. The positivity of H. pylori determined by serology in 70 patients (50%) was significantly higher than those determined by histology 22 patients (15.71%). No significant association between H. pylori infection and gastric cancer was observed.
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PMID:Association of Helicobacter pylori infection with gastric carcinoma. 1963 38

It has been clearly established that Helicobacter pylori (H. pylori) infection plays a pivotal role in the pathogenesis of chronic gastritis, peptic ulcer, gastric adenocarcinoma, and gastric lymphoma MALT (mucosa-associated lymphoid tissue) in the general population, but data regarding the prevalence and the role of H. pylori infection in liver cirrhosis are conflicting. Most serological studies estimated a high prevalence of H. pylori infection in patients with liver cirrhosis; however, when other methods (urea breath test, histology, culture, rapid urease test) were used, the overall H. pylori prevalence was similar to that in controls. Although the prevalence of both gastric ulcer (GU) and duodenal ulcer (DU) is higher in cirrhotic patients than in general population, the relationship between H. pylori infection and peptic ulcer in cirrhosis remains controversial. Our data regarding peptic ulcer prevalence in cirrhotic patients are in agreement with previous studies that suggest an increased prevalence of both GU and DU. The incidence of bleeding peptic ulcer is high in cirrhotic patients and carries an increased risk of complications or death in these patients and therefore eradication of H. pylori infection might be as effective in preventing ulcer relapse and bleeding as it is in noncirrhotic ulcer patients. Hepatic encephalopathy is a frecquent complication of liver cirrhosis, and it is widely accepted that ammonia plays a major role in its pathogenesis. The ammonia production by H. pylori urease does not increase blood ammonia levels during cirrhosis, and eradication of H. pylori infection does not affect hepatic encephalopathy status.
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PMID:[Prevalence and role of Helicobacter pylori infection in some gastroduodenal and hepatic complications in cirrhotic patients]. 2020 58


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