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Página 1 a partir de 61 resultados
(-)-Patchouli alcohol protects against Helicobacter pylori urease-induced apoptosis, oxidative stress and inflammatory response in human gastric epithelial cells.
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(-)-Patchouli alcohol (PA), the major active principle of Pogostemonis Herba, has been reported to have anti-Helicobacter pylori and gastroprotective effects. In the present work, we aimed to investigate the possible protective effect of PA on H. pylori urease (HPU)-injured human gastric epithelial
Papillary necrosis in vitro: a scanning electron microscopic comparison of escherichia coli and Proteus mirabilis infection.
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The effect of bacterial infection on excised renal papillae as a model for papillary necrosis and subsequent calcification was investigated. Sterile rat renal papillae were placed in 25 ml aliquots of filter sterilized human urine and then inoculated with one ml suspensions of sterilized human urine
Contribution of Proteus mirabilis urease to persistence, urolithiasis, and acute pyelonephritis in a mouse model of ascending urinary tract infection.
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Proteus mirabilis, a significant cause of bacteriuria and acute pyelonephritis in humans, produces urease. This high-molecular-weight, multimeric, cytoplasmic enzyme hydrolyzes urea to ammonia and carbon dioxide. To assess the role of urease in colonization, urolithiasis, and acute pyelonephritis in
Adoptive transfer of CD4+ T cells specific for subunit A of Helicobacter pylori urease reduces H. pylori stomach colonization in mice in the absence of interleukin-4 (IL-4)/IL-13 receptor signaling.
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Protection in the murine model of Helicobacter pylori infection may be mediated by CD4+ T cells, but the mechanism remains unclear. To better understand how protection occurs in this model, we generated and characterized H. pylori urease-specific CD4+ T cells from BALB/c mice immunized with
Ammonia as an accelerator of tumor necrosis factor alpha-induced apoptosis of gastric epithelial cells in Helicobacter pylori infection.
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The mechanism by which Helicobacter pylori induces apoptosis remains unclear. In a previous study using biopsy samples, we found a significant correlation between the urease activity of an H. pylori strain and the apoptosis level induced by this strain. Therefore, in this study, we investigated
Generation of ammonia and mucosal lesion formation following hydrolysis of urea by urease in the rat stomach.
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We examined the morphological changes in gastric mucosa and the generation of ammonia after exposure of the rat stomach to urea in the presence of urease, in attempts to investigate a pathophysiological role of urea, urease, and ammonia system in gastric ulcer diseases. Exposure of the stomach for
Potential phytotoxicity associated with the use of soil urease inhibitors.
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Recent work in our laboratory showed that the adverse effect of urea fertilizer on seed germination and seedling growth in soil is due to ammonia produced through hydrolysis of urea by soil urease (NH(2)CONH(2) + H(2)O --> 2NH(3) + CO(2)) and can be eliminated by amending the fertilizer with a small
Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy.
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Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by
Helicobacter pylori urease is a potent stimulus of mononuclear phagocyte activation and inflammatory cytokine production.
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OBJECTIVE
Helicobacter pylori surface proteins induce the production of proinflammatory mediators by mononuclear phagocytes, but the protein responsible for this stimulation has not been identified. This study determined whether urease, the major component of the soluble proteins extracted from H.
Cytokine expression and production by purified Helicobacter pylori urease in human gastric epithelial cells.
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Cytokines have been proposed to play an important role in Helicobacter pylori-associated gastroduodenal diseases, but the exact mechanism of the cytokine induction remains unclear. H. pylori urease, a major component of the soluble proteins extracted from bacterial cells, is considered to be one of
Recombinant Helicobacter pylori urease activates primary mucosal macrophages.
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Helicobacter pylori urease is absorbed into the gastric mucosa at sites of inflammation, but whether the enzyme activates mucosal macrophages is not known. Because mucosal macrophages differ phenotypically and functionally from blood monocytes, whether recombinant H. pylori urease (rUrease)
Auraptene attenuates gastritis via reduction of Helicobacter pylori colonization and pro-inflammatory mediator production in C57BL/6 mice.
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Helicobacter pylori is a major human pathogen that plays central roles in chronic gastritis and gastric cancer. Recently, we reported that auraptene suppressed H. pylori adhesion via expression of CD74, which has been identified as a new receptor for H. pylori urease. In this study, we attempted to
Increased Glycated Hemoglobin Levels in Patients With Helicobacter pylori Infection Are Associated With the Grading of Chronic Gastritis
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Background: Recent studies have found an association between Helicobacter pylori infection and prediabetes. Whether H. pylori per se or host factors are involved in the disturbance of glycated hemoglobin needs further
First Report of Rhizome Rot on Ginger (Zingiber officinale) Caused by Enterobacter cloacae in Shandong Province, China
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Ginger (Zingiber officinale Roscoe) is an economically important crop that is planted on 60,000 to 70,000 ha every year in Shandong Province, China. During June to July 2019, a bacterial disease was observed on ginger in Shandong Province. The disease incidence was about 15% in each of three fields
Helicobacter pylori infection, immune response and vaccination.
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It is well known that abnormal immune responses may play a pathogenic role in the H. pylori-related gastropathy. Indeed, as far as humoral immune response is concerned, it is still debated whether specific anti-H. pylori antibodies have a protective or noxious effect in infected hosts. Besides
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