Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The observation that activation of eosinophils in vitro with PAF increases the surface expression of the alpha chain of the complement receptor CR3 (CD11b) has been extended to other eosinophil activating factors. CD11b may be detected on activated eosinophils by reaction with mouse monoclonal anti-human CD11b IgG, following the addition of urease-conjugated sheep anti-mouse IgG. CD11b levels were increased on eosinophils after incubation with (a) recombinant colony stimulating factors, IL-3, GM-CSF and IL-5, at concentrations of 100 U/ml, or (b) with eosinophil activating factors, recombinant TNF alpha (1000 U/ml), EAF purified from mononuclear cell supernatants and PAF (10(-6) M). CD11b levels were not affected by IL-1 alpha, IL-2 or IFN-gamma. Unstimulated neutrophils had higher levels of CD11b than unstimulated eosinophils, but neutrophil CD11b was unaffected by IL-3, GM-CSF and IL-5 and was only slightly affected by TNF, EAF and PAF. Polyclonal rabbit antibodies to IL-3 and TNF neutralised their CD11b enhancing activities. The PAF antagonists WEB 2086 and WEB 2170 neutralised the CD11b enhancing activity of PAF. We conclude that measurement of CD11b expression on eosinophils is a convenient method for the assay of eosinophil activating activity.
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PMID:A new method for measuring eosinophil activating factors, based on the increased expression of CR3 alpha chain (CD11b) on the surface of activated eosinophils. 134 5

The pathogenesis of gastric carcinoma developing after infection with Helicobacter pylori now seems to be clear. The release of urease, alcohol dehydrogenase, enzymes and cytotoxin on the one hand, and chemotactic factors, PAF and heat-shock proteins on the other trigger chronic inflammation and epithelial metaplasia and dysplasia in the stomach. Under the influence of additional carcinogens, the epithelial changes progress to severe dysplasia and finally carcinoma. As a result of chronic inflammation, MALT lymphomas can also be induced. These can be made to regress by eradicating Hp. The possibility of being able to prevent up to 80% of the carcinomas of the stomach by eradicating Hp holds out good prospects, over the long-term, for the prevention of these tumors. Accurate identification of the patient groups carrying a high risk is now necessary.
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PMID:[MALT lymphoma, stomach carcinoma--role of Helicobacter pylori. Are chances for prevention on the horizon?]. 784 83

H. pylori organisms are microaerophilic gram-negative curved or spiral bacteria that live in the mucus layer of the gastric epithelium. Since the discovery of H. pylori similar organisms have been found in humans (H. cinaedi, H. fennelliae, H. heilmanii) and animals. H. pylori causes chronic active gastritis and is an important factor in the development of peptic ulceration and gastric cancer. Narrow host range, tissue specificity and chronic inflammation are characteristic features. Putative virulence factors of H. pylori are structural components (flagella, adhesins...) extracellular bacterial products (urease, protease, phospholipase, cytotoxin...), induction of autoimmune reactions and the activation or stimulation of cellular products (PAF, interleukins, TNF alpha...). Colonization with H. pylori is common throughout the world; it is likely that one half of the world's population is infected. In developed countries few infections occur during childhood, whereas in developing countries most persons are infected by the age of 10 years. Socioeconomic factors seem to determine the age of acquisition. Person to person spread is the most likely form of transmission, but it is not clear whether this is fecal-oral or oral-oral. No non-human reservoir has been identified so far.
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PMID:[Helicobacter pylori: pathogens, pathomechanisms and epidemiology]. 797 67

Ureases (EC 3.5.1.5) are highly homologous enzymes found in plants, bacteria and fungi. Canatoxin, an isoform Canavalia ensiformis urease, has several biological properties unrelated to its ureolytic activity, like platelet-aggregating and pro-inflammatory effects. Here, we describe that Bacillus pasteurii urease (BPU) also induces aggregation of rabbit platelets, similar to the canatoxin-induced effect (ED(50) 0.4 and 0.015 mg/mL, respectively). BPU induced-aggregation was blocked in platelets pretreated with dexamethasone and esculetin, a phospholipase A(2) and a lipoxygenase inhibitor, respectively, while platelets treated with indomethacin, a cyclooxygenase inhibitor, showed increased response to BPU. Methoxyverapamil (Ca(2+) channel blocker) and AMP (ADP antagonist) abrogated urease-induced aggregation, whereas the PAF-acether antagonist Web2170 had no effect. We concluded that platelet aggregation induced by BPU is mediated by lipoxygenase-derived eicosanoids and secretion of ADP from the platelets through a calcium-dependent mechanism. Potential relevance of these findings for bacterium-plant interactions and pathogenesis of bacterial infections are discussed.
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PMID:Bacillus pasteurii urease shares with plant ureases the ability to induce aggregation of blood platelets. 1683 15