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 and adenomatous polyposis coli (Apc) gene mutations have been linked to gastric cancer in humans, but possible synergistic interaction(s) between these risk factors have not been examined. Fourteen C57BL/6 wild-type and 14 Apc1638 heterozygous mice were inoculated with Helicobacter felis at 6 weeks of age and compared at various time points with a similar number of uninfected control mice of the same genotype. Both infected and uninfected Apc1638 mice had a limited incidence of atypical proliferation foci in the mucosa of the antrum and pyloric junction at 4.5 and 6 months of age, whereas polyps of the antrum and pylorus were present in all mice, regardless of infection status, at 7.5 months. In contrast, no altered gastric mucosal foci were observed in control or infected C57BL/6 mice at any time point. Interestingly, the infected Apc1638 mice had less epithelial proliferation and inflammation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the wild-type and Apc mutant mice had a Th1-like immune response, based on a predominantly IgG2a immunoglobulin response), and higher bacteria and urease scores than did infected wild-type C57BL/6 mice. In conclusion, the Apc1638 truncating mutation leads to gastric dysplasia and polyposis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead to an increased rate of gastric neoplasia. In addition, our data suggest this Apc mutation may actually lead to decreased immune, inflammatory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a novel role for this tumor suppressor gene in the immune and local tissue responses to gastric bacterial infection.
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PMID:Mice carrying a truncated Apc gene have diminished gastric epithelial proliferation, gastric inflammation, and humoral immunity in response to Helicobacter felis infection. 930 81

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.
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PMID:Decreased gastric proliferation of foveolar epithelial cells after the eradication of Helicobacter pylori. 936

The ideal approach for the initial diagnosis of Helicobacter pylori infection is to perform an endoscopy to obtain biopsy specimens for histology and culture. Histology allows classification of any gastritis lesions present and may have prognostic value, and culture enables susceptibility testing of antimicrobial agents to direct proper treatment. Biopsy specimens must also be taken from the corpus if the patient was pretreated with proton pump inhibitors. The cost of these tests and the delay in receiving results limits their use in clinical practice. Therefore, the urease test, a quick and inexpensive test, is used to detect the presence of H. pylori and constitutes the basic invasive test for H. pylori. A new urease test based on a strip instead of an agar disk may be the test of choice in the future, because of its increased sensitivity and 2-hour delay (instead of 24 hours) in obtaining the result. In some countries, because of the cost, endoscopy will be used in selected patients only, either because of alarm symptoms or age > 45 years, which is considered a threshold for gastric cancer risk. In other patients, the noninvasive tests will be used. The cost of serology makes it more attractive compared with the urea breath test. Currently, there are accurate enzyme-linked immunosorbent assay tests that can be performed in any laboratory and that provide precise and quick diagnoses. In the event of a doubtful result, an immunoblot can be performed, as is the case for other infections. Patient follow-up after treatment provides a different situation because bacterial load is usually lower. A noninvasive test should be performed, and only the urea breath test can be used within the timing originally proposed to test eradication efficacy (i.e., 4-6 weeks after treatment). If the result is positive, susceptibility testing is required before administering a second course of treatment. The increasing use of antimicrobial agents to treat H. pylori is likely to result in antimicrobial resistance, requiring that bacteriologic surveillance programs be implemented. There are numerous research projects ongoing in this area, and one can expect that improved methods, such as colorimetric polymerase chain reaction (PCR) and improved antibody tests, will also be used in the future.
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PMID:How should Helicobacter pylori infection be diagnosed? 939 68

Multiple invasive and noninvasive tests for detecting Helicobacter pylori infection are available. The current "gold standard" for the diagnosis of H. pylori infection requires histology and the rapid urease test. Our aim was to test the performance of immunoglobulin A (IgA) and IgG immunoblot assays in comparison with that of the gold standard tests for the diagnosis of H. pylori infection. Ninety patients who underwent gastroscopy were analyzed in a prospective study. Fifty-nine of them were defined to be H. pylori positive by the gold standard tests. The IgA and IgG immunoblot assays correctly identified H. pylori infection in 17 and 58 of these patients, respectively, indicating that determination of IgA antibodies seems to be of low diagnostic value for H. pylori infection. In contrast, the sensitivity and specificity of the IgG immunoblot assay were 98 and 71%, respectively, with positive and negative predictive values of 87 and 96%, respectively. Therefore, the IgG immunoblot assay proved to be a sensitive and useful, noninvasive test for the diagnosis of H. pylori infection.
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PMID:Use of serum-specific immunoglobulins A and G for detection of Helicobacter pylori infection in patients with chronic gastritis by immunoblot analysis. 939 94

Helicobacter pylori infection is mainly acquired in childhood, and studies on the epidemiology of this infection depend on the availability of a noninvasive diagnostic test for use in children. The aim of this study was to determine whether the carbon 13-labeled urea breath test (UBT) can be used in children by evaluating: (1) its sensitivity and specificity compared with either culture or both rapid urease test and histologic examination, (2) whether a test meal or a prolonged fast is required, (3) the usefulness after treatment for H. pylori. Eighty-eight children (mean age, 10.6 +/- 4.19 years) who were undergoing upper endoscopy were studied while fasting, not fasting, and after treatment. Children were given 50 mg of 13C-urea if they weighed less than 50 kg or 75 mg of 13C-urea if they weighed more than 50 kg with 50 mg of a glucose polymer solution in 7.5 ml of water. Breath samples were collected at baseline and at 15, 30, 45, and 60 minutes. In 63 fasting children the UBT was 100% sensitive and 97.6% specific at 30 minutes with a cutoff value of 3.5 delta 13CO2 per mil. Nonfasting tests in 23 children, performed between 1 and 2 hours after their usual meal, were 100% sensitive and 91.6% specific. In 13 children fed directly before the UBT, the sensitivity of the test was reduced to 50%. Thirty minutes was the optimal sampling time. There was a significant decrease in specificity when samples were obtained at 15 minutes, possibly caused by the interference of oral urease-producing organisms. The test was 100% sensitive and specific in 20 children after treatment for H. pylori infection. The UBT is a highly sensitive and specific test for the diagnosis of H. pylori infection in children. Neither a prolonged fast nor a test meal is required.
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PMID:Carbon 13-labeled urea breath test for the diagnosis of Helicobacter pylori infection in children. 942 77

In order to study a possible role of Helicobacter pylori infection in chronic laryngitis, we performed endoscopic and histological assessments in addition to a urease test for the bacterium in 35 patients with chronic hoarseness. Six of the patients investigated (17.1%) revealed a positive urease test of the laryngeal biopsy (four male and two female patients). These H. pylori-positive patients were treated with omeprazole and an antibiotic regimen using clarithromycin and metronidazole. This led to an eradication of the H. pylori and resolution of clinical signs and symptoms. These findings show a possible role of H. pylori infection in the etiology of chronic laryngitis in certain patients and can be important for clinical diagnosis and treatment.
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PMID:A possible role of Helicobacter pylori infection in the etiology of chronic laryngitis. 943 24

Mucosal vaccination using different antigens in conjunction with adjuvants has been used for the prevention and even cure of Helicobacter infection in animal models. A phase I-II trial was recently performed on infected volunteers with urease and the heat labile enterotoxin from E. coli (LT). A significant decrease in bacterial density but no cure of infection was observed in some patients. The immune effectors which prevent or cure infection with Helicobacter are not well understood and will need to be more clearly defined in order to improve vaccination strategies. Future developments will likely include the following: generation of new mucosal adjuvants without gastrointestinal toxicity; combination of two or three different antigens in order to ensure broader efficacy; use of different routes of administration such as nasal or rectal; coadministration of anti-Helicobacter treatment and vaccine; development of alternate vaccine methods which do not require a mucosal adjuvant, i.e. antigen expression by live carriers or by DNA vaccination; combination of different vaccination methods, for instance DNA vaccination followed by a mucosal boost.
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PMID:Perspectives of anti-H. pylori vaccination. 944 56

Live Salmonella typhimurium phoPc bacteria were tested as mucosal vaccine vectors to deliver Helicobacter pylori antigens. The genes encoding the A and B subunits of H. pylori urease were introduced into S. typhimurium phoPc and expressed under the control of a constitutive tac promoter (tac-ureAB) or a two-phase T7 expression system (cT7-ureAB). Both recombinant Salmonella strains expressed the two urease subunits in vitro and were used to nasally immunize BALB/c mice. The plasmid carrying cT7-ureAB was stably inherited by bacteria growing or persisting in the spleen, lungs, mesenteric or cervical lymph nodes, and Peyer's patches of immunized mice, while the plasmid carrying tac-ureAB was rapidly lost. Spleen and Peyer's patch CD4+ lymphocytes from mice immunized with S. typhimurium phopc cT7-ureAB proliferated in vitro in response to urease, whereas cells from mice given S. typhimurium phoPc alone did not. Splenic CD4+ cells from mice immunized with phoPc cT7-ureAB secreted gamma interferon and interleukin 10, while Peyer's patch CD4+ cells did not secrete either cytokine. Specific H. pylori anti-urease immunoglobulin G1 (IgG1) and IgG2A antibodies were detected following immunization, confirming that both Th1- and Th2-type immune responses were generated by the live vaccine. Sixty percent of the mice (9 of 15) immunized with S. typhimurium phoPc cT7-ureAB were found to be resistant to infection by H. pylori, while all mice immunized with phoPc tac-ureAB (15 of 15) or phoPc (15 of 15) were infected. Our data demonstrate that H. pylori urease delivered nasally by using a vaccine strain of S. typhimurium can trigger Th1- and Th2-type responses and induce protective immunity against Helicobacter infection.
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PMID:Mice are protected from Helicobacter pylori infection by nasal immunization with attenuated Salmonella typhimurium phoPc expressing urease A and B subunits. 945 12

The peptic ulcer of gastric tube using for esophageal reconstruction is rare. We report herein five cases of peptic ulcer of gastric tube used for esophageal reconstruction after esophagectomy for esophageal carcinoma. The reconstructive route, in all cases, was posterior mediastinum. In one case, 10 days after esophagectomy, he had high grade fever and pneumonia of right lower lobe of lung. Endoscopic examination revealed a deep ulcerative lesion on anterior wall of gastric tube and fistula formation on membranous part of trachea. The partial resection of gastric tube was performed for closing to tracheo-gastro fistula. In other four cases, the location of ulcer was middle or lower third of gastric tube. One had multiple peptic ulcer and other had single. Two cases of four underwent post irradiation therapy. One case of then, the Helicobacter infection detected using by rapid urease test and histological examination. We analyzed of Helicobacter pylori infection and serum gastrin level of gastric tube in outpatients who have used gastric tube for esophageal reconstruction after radical esophagectomy. Helicobacter pylori infection was positive at 56% (9/16) of all patients. The serum gastrin level of patients who was positive of Helicobacter pylori infection is not significantly higher than that of patients who was negative. We consider that post operative irradiation therapy and Helicobacter infection might play in development of peptic ulcer of gastric tube.
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PMID:[Five cases of peptic ulcer of gastric tube after radical esophagectomy for esophageal carcinoma and analysis of Helicobacter pylori infection at gastric tube]. 945 13

The urea breath test (UBT) has been shown to be a reliable non-invasive method for detection of H. pylori infection. There is widespread use of a test meal in the 13C UBT, but to what extent exclusion of the test meal actually influences the accuracy of the test has been poorly investigated. In addition, there is variability between test protocols in breath sampling frequency. In this evaluation, 91 patients with dyspeptic symptoms were investigated in an out-patient endoscopy ward, using a simplified 13C UBT without a test meal, and a single point breath evaluation after ingestion of 13C-labelled urea. Helicobacter pylori infection was diagnosed on upper endoscopy by histology and rapid urease tests on biopsies from the antrum and corpus mucosa of the stomach. Fifty-four percent of the patients had H. pylori infection. With the chosen cut-off level, the sensitivity and specificity of the 13C UBT were 92% and 95%, respectively. We conclude that this simplified 13C UBT is easy to perform and a very reliable test for detecting H. pylori infection, making it a suitable test in routine clinical work.
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PMID:Accurate detection of Helicobacter pylori infection with a simplified 13C urea breath test. 945 91


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