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)

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 proinflammatory cytokines released from macrophages, such as tumor-necrosis factor-a and interleukin-1beta, and IFN-gamma derived from T-helper 1 lymphocytes, also interleukin-10, a product of T-helper 2 lymphocytes with antiinflammatory properties, seems to be surprisingly involved in the pathogenesis of H. pylori-induced gastritis. In addition, lipopolysaccharide derived from the outher membrane of H. pylori acts as a chemoattractant for monocytes and induces release of free radicals, interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha. On the other hand, H. pylori lipopolysaccharide could be responsible for the increased polyamine concentrations in the gastric mucosa and polyamines, such as putrescine, spermidine and spermine, could be involved in the increased cell proliferation and consequent possible neoplastic transformation of the gastric mucosa. Incubation of peripheral blood mononuclear cells with H. pylori increases significantly the surface expression of CD95 receptor (Fas), thus suggesting that these bacteria are able to induce apoptosis. In animal models, different types of vaccination have been investigated, including stimulation of nasal and rectal lymphoid tissue, as well as adoptive transfer of T cell from donors immunized with H. pylori. However, results obtained are frequently disappointing. In humans, urease of H. pylori was safely used as oral vaccine in the absence or presence of adjuvants with encouraging results. Finally, DNA vaccines could offer in the future advantages for prophylactic H. pylori eradication, especially where population is infected by this microorganism since childhood.
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PMID:Helicobacter pylori infection, immune response and vaccination. 1247 86

Gastric Helicobacter pylori (Hp) infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis resulting from the long-term Hp infection but functional aspects accompanying this Hp-induced progression from gastritis to the cancer, especially changes in gastric acid secretion, gastric blood flow (GBF) and gastrin-somatostatin link have been little studied. It is unclear whether Hp eradication therapy alters the functional and the histopathological changes in this animal model of Hp-infection. We examined the effects of intragastric (i.g.) inoculation of Mongolian gerbils with Hp strain (cagA+ vacA+, 5 x 10(6) CFU/ml) that had been isolated from a patient with gastric ulcer as compared to those induced by vehicle (saline) in gerbils with or without gastric fistula (GF) at 1.2, 4, 6, 9, 12 and 30 wks upon gastric inoculation with this bacteria. An attempt was made to evaluate the influence of anti-Hp triple therapy with omeprazole, amoxicillin and tinidazol on gastric Hp-infection and Hp-induced functional impairment of the gastric mucosa. Gastric mucosal biopsy specimens were taken for the assessment of the morphological changes and the presence of Hp infection using rapid urease test (CLO-test) and the density of Hp-colonization were assessed by counting of the number of bacterial colonies per plate. Gastric blood flow (GBF) was measured by H2-gas clearance technique and the venous blood and the gastric content were collected for the measurement of plasma gastrin levels and the gastric luminal somatostatin level by radioimmunoassay (RIA). The Hp in gastric mucosa was detected in all animals by culture and rapid urease test at various periods upon Hp inoculation. Basal gastric acid in non-infected conscious gerbils with GF reached the level of about 28 +/- 4 micromol/h and this was reduced by over 50% immediately upon the Hp-inoculation and persisted for time intervals tested up to 30 wk. Early lesions were seen 4 wks after the Hp-inoculation and consisted of chronic gastritis with thickened gastric mucosal foldings and elongated interfoveolar ridges. Edema and congestion as well as significant mucosal inflammatory infiltration with lymphoid infiltrate in lamina propria of the mucosa occurred in all infected gerbils. Adenomatous hyperplasia with cellular atypia was observed at 12 wk upon Hp-inoculation together with increased mitotic activity and numerous apoptotic bodies formation, while lamina propria was reduced leaving dilated atypical gastric gland situated "back-to-back". This glandular atypia failed to show lamina propria or submucosa infiltration corresponding to gastric intraepithelial neoplasia. The GBF in Hp-infected gerbils was significantly lower, and a 6-7 fold increase in plasma gastrin levels combined with a significant fall in gastric luminal somatostatin contents observed at all tested periods as compared to vehicle-controls and these effects were counteracted by anti-Hp triple therapy. We conclude that: 1). Hp-infection in Mongolian gerbils in early stages before adenocarcinoma formation results in the development of typical functional and pathological changes such as suppression of gastric secretion and impairment of both, gastric mucosal microcirculation and gastrin-somatostatin link, and 2). this deleterious influence of Hp on gastric morphology and gastric functions is greatly attenuated in gerbils treated with Hp-eradication therapy.
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PMID:Triple eradication therapy counteracts functional impairment associated with Helicobacter pylori infection in Mongolian gerbils. 1267 17

The early consequences of Helicobacter pylori infection and the role of bacterial virulence determinants in disease outcome remain to be established. The present study sought to measure the development of host inflammatory and immune responses and their relationship to the putative bacterial virulence factors cag pathogenicity island (cagPAI), vacA allele, and oipA in combination with bacterial colonization density in a feline model of the early stages of H. pylori infection. Gastric tissues obtained from infected and uninfected cats were evaluated for H. pylori ureB, cagPAI, vacA allele, and oipA and colonization density (urease, histology, and real-time PCR). Inflammation was assessed by measuring mRNA upregulation of gamma interferon (IFN-gamma), interleukin (IL)-1 alpha, IL-1 beta, IL-4, IL-6, IL-8, IL-10, and IL-12 p40 and histopathology. The mucosal immune response was characterized by morphometric analysis of lymphoid follicles and by differentiating lymphocyte populations with antibodies against surface markers. Infecting H. pylori strains were positive for vacAs1 but lacked cagPAI and an active oipA gene. Colonization density was uniform throughout the stomach. Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and increased severity of inflammatory infiltrates and fibrosis were observed in infected cats. The median number and total area of lymphoid aggregates were 5 and 10 times greater, respectively, in the stomachs of infected than uninfected cats. Secondary lymphoid follicles in uninfected cats were rare and positive for BLA.36 and B220 but negative for CD3 and CD79 alpha, whereas in infected cats they were frequent and positive for BLA.36, CD79 alpha, and CD3 but negative for B220. Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and marked hyperplasia of secondary lymphoid follicles are early consequences of H. pylori infection in cats. The response appears to be similar to that of infected people, particularly children, can develop independently of the pathogenicity factors cagPAI and oipA, and is not correlated with the degree of colonization density or urease activity.
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PMID:Quantitative evaluation of inflammatory and immune responses in the early stages of chronic Helicobacter pylori infection. 1270 44

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.
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PMID:Functional dyspepsia: relationship between clinical subgroups and Helicobacter pylori status in Western Turkey. 1279 4

To date, two Helicobacter species, Helicobacter pylori and 'Helicobacter heilmannii' (formerly named 'Gastrospirillum hominis'), have been identified from the human stomach. In this study, we observed non-H. pylori-shaped bacteria in gastric tissue sections and successfully isolated them by cultivation. Elongated bacteria were isolated from a patient with gastric-mucosa-associated lymphoid-tissue lymphoma who had been diagnosed as H. pylori-negative by culture, rapid urease test and histopathology in another hospital. The bacteria were grown only on chocolate agar in a CO2 incubator, appeared more than 10 microm long in histological sections, formed small colonies and showed poor growth in a brain heart infusion broth; these characteristics apparently differed from common clinical isolates of H. pylori. However, the bacteria were identified as H. pylori by PCR of the urease gene, 16S rDNA sequencing, protein profile and antigenicity examined by anti-H. pylori polyclonal antibody. These observations suggest that the H. pylori strain identified in this study may contribute to the development of gastroduodenal diseases in cases judged as H. pylori-negative by ordinary methods.
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PMID:Characterization of elongated Helicobacter pylori isolated from a patient with gastric-mucosa-associated lymphoid-tissue lymphoma. 1497 Feb 45

Conjunctival mucosa-associated lymphoid tissue (MALT) lymphoma is an extranodal marginal zone B-cell lymphoma that is characterized by an exaggerated clonal expansion of B cells, which implicate a pathological proliferative response to antigen(s) including bacteria. Helicobacter pylori (H. pylori) infection is recognized as one of the causative agents of gastric MALT lymphoma; however, it has not been reported in extra gastric MALT lymphoma. We studied 5 patients (4 adults and 1 child) with salmon-colored conjunctival lesions. One patient also had a history of abnormal bone marrow biopsy a year earlier with lymphoid aggregates involving 5% of the overall bone marrow. The conjunctival lesions of the 5 patients were biopsied. Histopathological diagnoses were consistent with conjunctival MALT lymphoma. Lymphoma and normal conjunctival cells were microdissected using laser capture microscopy or manual techniques. DNA was extracted and subjected to PCR amplification using H. pylori gene-specific primers from the urease B and vac/m2 gene. Cells from chronic conjunctivitis (normal lymphocytes), conjunctival human T-cell lymphotropic virus type-1/adult T-cell leukemia/lymphoma (HTLV-1/ATL), and orbital B-cell lymphoma were also microdissected, processed and analyzed. PCR amplification and Southern blot hybridization demonstrated H. pylori DNA in the conjunctival MALT lymphoma cells of 4/5 cases. The negative case was the one with a history of abnormal bone marrow. In contrast, H. pylori gene was not detected in normal conjunctival cells from the cases of MALT lymphoma or the lymphocytes, ATL and orbital B-lymphoma cells from the controls. These data suggest that H. pylori may play a role in conjunctival MALT lymphoma.
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PMID:Helicobacter pylori (H. pylori) molecular signature in conjunctival mucosa-associated lymphoid tissue (MALT) lymphoma. 1537 65

A Toll-like receptor-4 (TLR-4) Asp299Gly and Thr399Ileu substitution reduces responsiveness to Helicobacter pylori (H. pylori) lipopolysaccharide. CagA+ strains of H. pylori are known to be associated with gastroduodenal diseases. Therefore we aimed to evaluate association of TLR-4 substitutions and CagA seropositivity with gastritis and precancerous lesions in a northern Indian population. After upper gastrointestinal endoscopy, 130 rapid urease test (RUT)-positive patients with nonulcer dyspepsia (NUD) were included. Patients with NUD were also screened for H. pylori infection using modified Giemsa staining and anti-CagA IgG enzyme-linked immunoabsorbent assay. All patients and 200 asymptomatic control subjects were genotyped for TLR-4 substitutions using polymerase chain reaction-restriction fragment length polymorphism. We observed that frequencies of TLR-4 Asp299Gly variants were comparable between patients and control subjects, and also between positive and negative groups of precancerous lesions in patients. Frequencies of TLR-4 399Ileu allele (8% vs 3%, p = 0.008) and Asp299-Ileu399 haplotype (6.5% vs 3%, p = 0.022) were higher in patients than in control subjects at risk for gastritis (OR = 2.6 and 2.5, respectively). TLR-4 399Ileu allele carriers had higher risk for plasma cell infiltration (p = 0.023, OR = 10.6) that led to atrophy (p = 0.028, OR = 4.2) and intestinal metaplasia (p = 0.009, OR = 4.7). CagA positivity was more frequently associated with lymphoid follicle formation (p = 0.033, OR = 2.53). In conclusion TLR-4 Thr399Ileu substitution may be a risk factor for gastritis and precancerous lesions. CagA positivity may be a risk factor for lymphoid follicle development but not for other precancerous lesions in a northern Indian population.
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PMID:Association of Toll-like receptor-4 (Asp299Gly and Thr399Ileu) gene polymorphisms with gastritis and precancerous lesions. 1808 69

Helicobacter pylori is an important pathogen worldwide. Accurate diagnosis and appropriate therapy is important in clinical practice. Invasive tests that accurately identify current infection include the biopsy urease test and histology. The best noninvasive tests for diagnosis include the urea breath test and stool antigen testing. Proton pump inhibitor therapy can lead to false-negative H. pylori test results, and treatment should be stopped for 1-2 weeks prior to testing if possible. In the setting of bleeding peptic ulcer disease, urea breath testing is recommended to rule out a false-negative biopsy test result if needed. The current recommendations for when to test for H. pylori vary around the world. Well-accepted indications include active and past ulcer disease, and gastric-mucosa associated lymphoid tissue lymphoma. There is no universal agreement regarding whether all patients with functional dyspepsia should be tested and treated, although this is an evidence-based recommendation. There is also evidence that H. pylori eradication prevents peptic ulcer disease in those starting NSAIDs long term. Primary treatment remains triple therapy with 10-14 days probably being superior to shorter courses of therapy. Quadruple therapy is recommended if standard triple therapy fails. Salvage therapies with levofloxacin, rifabutin or furazolidone have been identified. Novel approaches to treatment include sequential therapy and use of adjuvants.
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PMID:Helicobacter pylori: testing and treatment. 1907 36

The expression of growth factors, proteolytic enzymes, fibrogenic factors, and cytokines is altered in the Helicobacter pylori-infected gastric mucosa. Therefore, we aimed to evaluate the association of functional promoter variants of transforming growth factor (TGF)-B1 and matrix metalloproteinase (MMP)-7 genes with gastritis and gastric precancerous lesions. After upper gastrointestinal endoscopy, a total of 130 rapid urease test-positive patients with nonulcer dyspepsia were examined for H. pylori infection using modified Giemsa stain and IgG anti-CagA ELISA. All patients and 200 asymptomatic controls were genotyped for TGF-B1 (-509 C>T) and MMP-7 (-181 A>G) substitutions using PCR-RFLP. The genotype and allele frequencies of TGF-B1 and MMP-7 polymorphisms did not differ between patients and controls (p > 0.05). However, the CagA-positive patients with TGF-B1 -509 T allele had higher risk for gastric atrophy (p = 0.026, odds ratio [OR] = 2.38) and lymphoid follicle development (p = 0.028, OR = 2.29). In addition, CagA-positive patients carrying MMP-7 -181 G allele had risk for lymphoid follicle formation (p = 0.027, OR = 2.30). Thus, the present study revealed significant association of functional MMP-7 and TGF-B1 gene variants toward susceptibility to H. pylori-induced precancerous gastric lesions.
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PMID:Transforming growth factor-B1 and matrix metalloproteinase-7 promoter variants induce risk for Helicobacter pylori-associated gastric precancerous lesions. 1931 20

"Helicobacter heilmannii" ("H. heilmannii"), which belongs to the genus Helicobacter, is a group of bacterial species that display a long spiral-shaped morphology. Recent studies have demonstrated that "H. heilmannii" type 1 is actually H. suis, which mainly colonizes the stomachs of various animals and humans. However, the influence of H. suis on gastric diseases remains to be fully elucidated. In this report, we revealed the relationship between natural H. suis infection and follicular gastritis in the pig stomachs. From sequence analysis of the 16S rRNA, urease A, and urease B genes, the presence of H. suis was confirmed in pig gastric lymphoid follicles, and this bacterium was named H. suis KB1. In addition, H. suis KB1 was inoculated into C57BL/6J mice, and the following mouse model of the pathogenesis of follicular gastritis by H. suis infection was established: H. suis KB1 colonizes the mouse stomach, and moreover, induces the development of lymphoid follicles and acquired immune responses characterized by the activation of B cells and CD4 positive cells. These results may lead to better understanding of the relationship between H. suis and gastric diseases, especially follicular gastritis; and furthermore, our findings emphasize the zoonotic aspects of animal-human infection by H. suis.
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PMID:Helicobacter suis KB1 derived from pig gastric lymphoid follicles induces the formation of gastric lymphoid follicles in mice through the activation of B cells and CD4 positive cells. 2139 35


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