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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer.Materials and Methods. Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin-layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin.Results. Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication.Conclusions. This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Availability of the essential nutrient iron is thought to vary greatly in the gastric mucosa, and thus the human gastric pathogen Helicobacter pylori requires regulatory responses to these environmental changes. Bacterial iron-responsive regulation is often mediated by Ferric Uptake Regulator (Fur) homologs, and in this study we have determined the role of H. pylori Fur in regulation of H. pylori iron uptake.Methods. Wild-type H. pylori and fur mutant derivatives were compared after growth in iron-restricted and iron-replete conditions. Iron-uptake was measured using 55Fe-labeled iron, whereas gene expression was monitored at the transcriptional level using Northern hybridization and lacZ reporter gene fusions.Results. Iron-uptake and total cellular iron content were approximately five-fold increased in the fur mutant compared with the wild-type strain, which indicated that in the fur mutant iron-uptake is not repressed by excess iron. A comprehensive screening of all H. pylori genes encoding putative iron-uptake proteins indicated that some of these H. pylori genes are constitutively expressed, while others are iron- and Fur-regulated.Conclusions. Iron uptake in H. pylori is in part differently regulated compared with other bacteria, since in H. pylori some iron-uptake systems are constitutively expressed. However, other iron uptake systems of H. pylori display the iron- and Fur-mediated repression that is common in bacteria. Taken together, this Fur-mediated modulation of iron-uptake capacity may be a specific adaptation to the conditions in the human stomach, where iron starvation and iron overload can be encountered in relatively short time intervals.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. cag pathogenicity island is reported to be a major virulence factor of Helicobacter pylori. The aim of this study was to investigate the status of cag pathogenicity island genes and gastric histology in Korean children with H. pylori gastritis.Methods. Helicobacter pylori DNA was extracted from antral biopsy specimens from 25 children with H. pylori gastritis. Specific polymerase chain reaction assays were used for four genes of cag pathogenicity island. The features of gastritis were scored in accordance with the updated Sydney System.Results. cagA was present in 23 (92%) of 25 children, and cagE in 24 (96%). Twenty-two (88%) children were cagT positive and 19 (76%) virD4 positive. All of the selected genes of the cag pathogenicity island were present in 17 (68%) children and completely deleted in one child. There were no differences in neutrophil activity and chronic inflammation between children infected with intact cag pathogenicity island strains and those with partially or totally deleted-cag pathogenicity island strains.Conclusion. cag pathogenicity island is not a uniform, conserved entity in Korea. Completeness of cag pathogenicity island may not be the major factor to determine the severity of H. pylori gastritis in children.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Objective. Helicobacter pylori is implicated in gastric carcinogenesis through increased gastric epithelial cell turnover. In fact, high proportions of proliferating and apoptotic epithelial cells are found in H. pylori-infected gastric mucosa. E2F, a transcription factor, induces coordinated transactivation of a set of genes involved in cell cycle progression. The aim of this study was to investigate the expression of E2F in H. pylori-infected gastric mucosa and examine the correlation between such expression and gastric epithelial cell proliferation and apoptosis.Methods. Twenty-five patients with H. pylori-associated gastritis (HAG) and 13 control subjects negative for H. pylori were examined. E2F expression was studied in situ by Southwestern histochemistry, a method used to localize transcription factors. Labeled double-stranded oligo-DNA with specific consensus sequence for E2F binding sites was reacted with frozen sections from antral biopsy specimens obtained at endoscopy. Gastric epithelial cell proliferation was assessed by immunostaining of proliferating cell nuclear antigen (PCNA), while apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The percentages of epithelial cells with nuclear staining for PCNA and E2F were expressed as a positivity index (PI). The percentage of TUNEL-positive epithelial cells was defined as apoptotic index.Results. E2F was expressed in the nuclei of gastric epithelial cells within gastric pits. E2F PI in H. pylori-infected gastric mucosa was significantly higher than that in noninfected. Expression of E2F correlated well with PCNA-positive epithelial cells. We also demonstrated colocalization of PCNA with E2F expression in the same epithelial cells. Apoptotic index was also high in H. pylori-infected mucosa, and correlated with E2F PI.Conclusion. Our results demonstrated a significant increase in the expression of E2F in H. pylori-infected mucosa, which correlated with both the percentages of PCNA- and TUNEL-positive cells. Our results suggest that enhanced E2F expression in gastric mucosa may be involved in H. pylori-related gastric carcinogenesis through accelerated cell turnover.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Bacteria have different characteristics in stimulation of human neutrophils to produce reactive oxygen species (ROS) and chemokines. This study examined the ability of Helicobacter pylori to induce production of ROS and chemokines by human neutrophils.Methods. H. pylori strains (1.5 × 108 CFU/ml) were cocultured with 5 × 104 neutrophils isolated from healthy subjects. Samples were incubated with human serum with or without IgG antibodies to H. pylori. ROS production was measured using luminol-dependent chemiluminescence (LmCL), and the concentrations of chemokines (IL-8, RANTES, MIP-1α and MCP-1) were measured by ELISA.Results. The mean of the highest LmCL (peak height; PH) value stimulated by H. pylori was 3318 in the absence of serum. PH increased to 4687 when incubated with anti-H. pylori antibody-positive sera (p 〈 .001) but antibody-negative sera did not affect LmCL response. The mean final concentration of IL-8 produced in the absence of serum was 142.6 pg/ml. Increased IL-8 production was seen by addition of antibody positive serum (p 〈 .01). IL-8 production was not significantly correlated with production of ROS. On the other hand, H. pylori stimulation did not induce neutrophil production of RANTES, MIP-1α or MCP-1.Conclusions. H. pylori was capable of inducing IL-8 production by human neutrophils, but not C-C chemokines. Production of C-X-C dominant chemokine by neutrophils is consistent with the pathological characteristics of H. pylori-induced gastritis, where persistent neutrophil infiltration is present.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Even after partial gastrectomy, Helicobacter pylori may persist in the residual stomach but be less abundant in the bacterial load. H. pylori stool antigen is a reliable noninvasive tool to detect H. pylori infection in patients without gastrectomy. We thus test whether [1] the course of H. pylori eradication therapy could be diminished [2]; stool antigen can effectively detect H. pylori infection for the patients with gastrectomy.Methods. One hundred and eight patients who had undergone partial gastrectomy were enrolled to receive panendoscopy and provided stool samples for H. pylori stool antigen within 3 days after endoscopy. The H. pylori-infected patients were then randomized to receive either a 3- or 7-day triple therapy for H. pylori eradication. Six weeks later, to evaluate the success of H. pylori eradication, patients received a follow-up endoscopy and again provided stool samples for H. pylori stool antigen.Results. Seventy out of 108 patients, proven to have H. pylori infection, were evenly randomized into 3-day and 7-day therapy groups. The H. pylori eradication rates were similar between the 3-day and 7-day triple therapy (90.9 vs. 93.8%, p 〉 .05). Before therapy, the H. pylori stool antigen was 93% sensitive and 100% specific to detect H. pylori. After therapy, H. pylori stool antigen remain 100% sensitive and 88.3% specific to detect the failure of eradication therapy.Conclusion. H. pylori stool antigen is a highly reliable tool to screen H. pylori infection before therapy and to assess the success of eradication therapy in partial gastrectomy patients. To eradicate H. pylori infection for patients with partial gastrectomy, the duration of triple therapy can be shortened.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. It has been proposed that Helicobacter pylori infection is related to cardiovascular disease, although this has not been fully investigated. The aim of this study was to investigate whether H. pylori in-fection is associated with cardiovascular risk factors.Subjects and Methods. One thousand six hundred and fifty people undergoing annual medical checks at Shimane Institute of Health Science between September 1998 and August 1999 were enrolled. Gender, age, body mass index, habitual smoking and drinking, systolic and diastolic blood pressure, serum level of total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDLC), blood glucose, leukocyte count and hemoglobin were compared between H. pylori seropositive and seronegative cases.Results. In H. pylori seropositive individuals, HDLC was significantly lower than that in seronegative individuals. After adjustment for possible confounding factors (gender, age, BMI, smoking and drinking habits), mean HDLC in H. pylori-seropositive and seronegative individuals were 56.1 and 58.2 mg/dl, respectively (p 〈 .005). The percentage of the elderly (over 50 years old) individuals with HDLC 〈 35 mg/dl in H. pylori seropositive and seronegative groups were 7.4% and 4.7%, respectively (p 〈 .001). In addition, the lower HDLC level was accompanied by an increased leukocyte count.Conclusion. Long-term infection with H. pylori may have an important role in decreasing the serum HDLC concentration.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Nitric oxide (NO) generated by nitric oxide synthase (NOS) is known to be an important modulator of the mucosal inflammatory response. In this study, we questioned whether Helicobacter pylori infection could up-regulate the epithelial cell inducible NOS (iNOS) gene expression and whether NO production could show polarity that can be regulated by immune mediators.Materials and Methods. Human gastric epithelial cell lines were infected with H. pylori, and the iNOS mRNA expression was assessed by quantitative RT-PCR. NO production was assayed by determining nitrite/nitrate levels in culture supernatants. To determine the polarity of NO secretion by the H. pylori-infected epithelial cells, Caco-2 cells were cultured as polarized monolayers in transwell chambers, and NO production was measured.Results. iNOS mRNA levels were significantly up-regulated in the cells infected with H. pylori, and expression of iNOS protein was confirmed by Western blot analysis. Increased NO production in the gastric epithelial cells was seen as early as 18 hours postinfection, and reached maximal levels by 24 hours postinfection. The specific MAP kinase inhibitors decreased H. pylori-induced iNOS and NO up-regulation. After H. pylori infection of polarized epithelial cells, NO was released predominantly into the apical compartment, and IL-8 was released predominantly into basolateral compartment. The addition of IFN-γ to H. pylori-infected polarized epithelial cells showed a synergistically higher apical and basolateral NO release.Conclusion. These results suggest that apical NO production mediated by MAP kinase in H. pylori-infected gastric epithelial cells may influence the bacteria and basolateral production of NO and IL-8 may play a role in the tissue inflammation.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Helicobacter pylori adhering to the human gastric epithelium causes gastric diseases such as ulcer, carcinoma and lymphoma. It is thus important to observe in detail both the surface of the epithelial cells and the H. pylori that adhered to it for the elucidation of H. pylori-induced diseases by scanning electron microscopy (SEM). Since the thick mucus layer blocks the observation of the cell surface and the bacteria, it is generally eliminated during the processing for SEM by roughly mechanical methods, but these treatments also demolish the ultrastructure of the cells. We studied the nonmechanical method for removal of mucus layer of gastric epithelium using pronase.Materials and Methods. To determine the optimal concentration of pronase, mucin was used as a substrate for inhibition of the viscosity. Pronase was added in 2% mucin at the concentration of 10, 50, 100, 500, 1000, 2000 or 5000 unit/ml and the flowing time of the mixture was measured. Based on the digestion experiment, biopsied specimens from 24 patients with dyspepsic symptoms were fixed in glutaraldehyde and then washed in rolling with different concentration of pronase. After the pretreatment by pronase, the specimens were treated according to the standard process for SEM.Results. We succeeded in removing the mucus layer on the surface of epithelial cells from the biopsied specimens fixed in glutaraldehyde by rinsing with 2000 unit/ml pronase for 24 hours.Conclusions. Using our digestive method without destroying the ultrastructure, the earliest stage which H. pylori has adhered onto the human gastric epithelium can be observed for the investigation of H. pylori-induced gastric disorders by SEM.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. The cag pathogenicity island (cag PAI) is a major virulence factor. The ability of Helicobacter pylori to adhere to gastric epithelial cells is an important initial step for virulence. The aim of this study was to evaluate the relationship between genetic variations of cag PAI in Japanese clinical isolates and the ability of H. pylori to adhere to gastric epithelial cells.Materials and Methods. The polymerase chain reaction and Southern blot analysis were used to verify the presence or absence of cagA, cagE, cagG, cagI and cagM in the cag PAI in 236 Japanese clinical isolates. The ability of H. pylori to adhere to KATOIII cells was examined by flow cytometry.Results. Seven (3.0%) cag PAI partial-deleted strains were found in 236 clinical isolates, and these strains showed three patterns in the deleted region within the cag PAI. All of the cagG-deleted strains showed decreased adherence to KATOIII cells, in comparison with cagG-positive strains. These strains had abolished IL-8 induction despite the presence of cagE, which is essential for IL-8 induction.Conclusions. Our results suggest that cagG or surrounding genes in the cag PAI has a function related to adhesion to epithelial cells.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Objective. To evaluate the efficacy of two commonly employed treatments for Helicobacter pylori infection and the impact of bacterial resistance to antibiotics on eradication rate.Methods. Ninety-two consecutive H. pylori-positive patients with active peptic ulcer disease were randomly enrolled to receive a 7-day treatment with either lansoprazole 30 mg plus amoxicillin 1 g and clarithromycin 500 mg [all twice a day (b.i.d.), Group A, n = 46]; or bismuth subcitrate 125 mg four times a day (q.i.d.) plus tetracycline 500 mg q.i.d and furazolidone 200 mg b.i.d. (Group B, n = 46) H. pylori status was reassessed 30 days after completion of the therapy and bacterial resistance to the antibiotics was investigated using an in vitro assay.Results. Five patients from each study group were lost to follow up. Both treatments resulted in similar H. pylori eradication rate: 66–60% (per protocol), 59–52% (intention-to-treat) in Groups A and B, respectively (non significant). However, eradication improved to 79% in the absence of H. pylori resistance to clarithromycin or amoxicillin.Conclusion. Primary resistance to clarithromycin or amoxicillin may underscore a potentially serious problem for the eradication of H. pylori infection. Testing for bacterial resistance may become necessary to improve therapeutic efficacy.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

The primary source of ammonia is the gut. Ammonia can also be generated by the urease activity of Helicobacter pylori in the gastric mucosa. The aim of this study was to investigate the effect of H. pylori eradication on blood and gastric juice ammonia levels and on visual evoked potential (VEP) recordings in cirrhotic patients.〈section xml:id="abs1-3"〉〈title type="main"〉Materials and Methods.Male patients with cirrhosis and H. pylori infection were prospectively evaluated. All patients were given triple regimen for eradication for 10 days. Gastroscopy together with gastric juice sampling for ammonia and mucosal sampling for H. pylori status was performed before and after therapy. Gastric juice and blood ammonia levels were measured and VEP recordings were obtained before and after treatment.〈section xml:id="abs1-4"〉〈title type="main"〉Results.Twenty-seven patients were included in the study. Patients with overt clinical hepatic encephalopathy were excluded from the study. Twenty-four out of twenty-seven patients became H. pylori-negative after the treatment. Ammonia measurements and VEP recordings were evaluated in the 24 patients in whom eradication was successful. A slight but statistically significant decrease in blood and a considerable decrease in gastric juice ammonia levels were observed after treatment [from 44.23 µmol/l to 41.6 µmol/l compared with 3234 µmol/l to 2709 µmol/l, respectively (p 〈 .05)] in patients in whom H. pylori was eradicated. VEP recordings were abnormal in 14 out of 24 patients before the treatment. Only four of these 14 patients with abnormal recordings showed improvement. (p 〉 .05).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions. Helicobacter pylori eradication in cirrhotics decreases blood and gastric juice ammonia concentrations whereas it does not provide an improvement in VEP recordings.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

The role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study.〈section xml:id="abs1-3"〉〈title type="main"〉Methods.Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status.〈section xml:id="abs1-4"〉〈title type="main"〉Results. Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, with adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing an oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12–0.67). Current smokers had an odds ratio of 17.3 (95% CI: 3.0–99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15–29.9). High alcohol consumption was no longer significantly associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46–3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% CI: 0.00–1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% CI: 0.14–1.2).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions. Helicobacter pylori infection is associated with a decreased risk of developing an oesophageal malignancy. Current smokers and ex-smokers have instead a definite increased risk of oesophageal neoplasms.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

In preparation of the approval of Helicobacter pylori therapy by the Japanese national health system, the board of directors of the Japanese Society for Helicobacter Research decided to prepare guidelines on the diagnosis and treatment of H. pylori infection for physicians in routine medical practice.〈section xml:id="abs1-3"〉〈title type="main"〉Methods.A guidelines preparation committee was formed and six meetings were held. Then, in December 1999, a consensus meeting was held in Kobe to obtain the opinions of general practitioners as well as experts from Europe, North America, and Asia.〈section xml:id="abs1-4"〉〈title type="main"〉Results. Helicobacter pylori eradication therapy is recommended in gastric or duodenal ulcer patients. Helicobacter pylori eradication therapy is recommended or gastric mucosa associated lymphoid tissue (MALT) lymphoma but it should be done at specialist institutions. The significance of H. pylori eradication therapy is still under evaluation in patients with hyperplastic polyps, chronic atrophic gastritis, non-ulcer dyspepsia and in patients after endoscopic mucosal resection of gastric cancer and after gastrectomy for gastric cancer. When diagnosing H. pylori infection, at least one of the tests requiring endoscopic biopsy (e.g. rapid urease test, histology, or culture) and tests not requiring biopsy (e.g. measurement of H. pylori antibody or urea breath test) should be used. Multiple tests are recommended to increase the accuracy. The drugs of first choice currently covered by the national health insurance system in Japan are: lansoprazole (30 mg) 1 capsule twice daily, amoxicillin (250 mg) 3 capsules twice daily, and clarithromycin (200 mg) 1–2 tablets twice daily. These three drugs should be administered after breakfast and dinner for 1 week.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion.These guidelines are intended for utilization in routine medical practice after the Japanese national health system begins to cover the management of H. pylori infection.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background. Helicobacter pylori infection is primarily acquired in childhood. However, the association between H. pylori infection and recurrent abdominal pain (RAP) remains unclear.Materials and methods. One hundred and forty-one children with and 21 without RAP underwent upper gastrointestinal endoscopy. At least five antral gastric biopsies were obtained from each patient and the presence of H. pylori infection was accepted when at least two out of four tests (histology, direct antral smear, culture, and rapid urease test) were positive. Patients with H. pylori infection underwent triple therapy with omeprazole, clarithromycin, and metronidazole.Results. Eighty-five out of 141 (60.3%) patients with RAP were H. pylori positive whereas 5 out of 21 (20.8%) patients without RAP were (p = .0037). Symptoms were disappeared in 87% of children whose H. pylori infection was eradicated compared with 41% of those in whom the infection was not eradicated (p = .0035).Conclusions. It was concluded that children with RAP and H. pylori infection appear to benefit from eradication therapy in Turkey.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

In this issue, Gisbert et al. (pp. 157–62) present the results of a noncomparative study evaluating a twice daily, 5-day regimen of ranitidine bismuth citrate, amoxicillin, clarithromycin and metronidazole twice daily for Helicobacter pylori cure. This study is one of a few stuides that evaluate a 5-day triple antimicrobial regimen in combination with a antisecretory agent. Although the study design precludes making any definite conclusion, it does encourage additional investigation of these types of regimens. Randomized controlled trials (RCTs) using regimens containing multiple agents should consider both standard-of-care comparator regimens and comparator regimens that will provide a better understanding of why regimens are more effective or better tolerated. The goal of treatment should be to maintain a lower bound 95% confidence interval (CI) of the point estimate of greater than 80% and a ‘delta’ (lower bound 95% CI of the difference in rates) of less than 10%. All RCTs should conduct susceptibility testing to evaluate the impact of resistance on efficacy and explain eradication failures. Finally, consideration should be given to the inclusion of patients with functional dyspepsia in H. pylori studies evaluating H. pylori cure since patients with peptic ulcer disease are becoming harder to find.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Helicobacter pylori is a neutralophilic bacterium that colonizes the acidic human gastric surface using the neutralizing capacity of a constitutively produced urease. Urease is present both in the cytoplasm and bound to the outside surface of the bacteria. The origin of the surface urease continues to be controversial. This study provides additional evidence that the origin of surface urease is cell lysis, not secretion.〈section xml:id="abs1-3"〉〈title type="main"〉Methods. H. Pylori was transformed with a plasmid encoding green fluorescent protein (GFP), a non-native cytoplasmic protein. Cultures supplemented with β-cyclodextrin or horse serum were collected over various time periods and spun through a ficoll cushion to gently separate whole bacteria from released protein. The pellet and supernatant fractions were analyzed by fluorimetry, SDS-PAGE and Coomassie blue or Western analysis.〈section xml:id="abs1-4"〉〈title type="main"〉Results.GFP fluorescence and antigenic reactivity in the supernatant increased at each time point. GFP, the non-native cytoplasmic protein, and UreB, a native cytoplasmic protein, increased over time in the supernatant and both proteins were always present in the pellet fraction. UreI, an inner membrane protein, was only present in the pellet fraction. β-galactosidase, a protein not found in H. pylori, was used as a negative control.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions.Since it is unlikely that there is an intrinsic secretion system for GFP, a non-native protein, its increasing presence over time in the supernate fraction along with UreB, and retention of UreI in the pellet fraction implies that cell lysis accounts for the presence of urease on the surface of H. pylori.

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1523-5378

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

 Clarithromycin-resistant Helicobacter pylori (CRHP) has increasingly been isolated from patients in Japan. The aim of our study was to test whether proton pump inhibitors (PPIs) and their thioether derivatives, which are secreted into the gastric mucosa, could inhibit the growth and motility (a factor in colonization) of CRHP.〈section xml:id="abs1-3"〉〈title type="main"〉Materials and Methods. CRHP was isolated from patients who had experienced gastritis or peptic ulcers in Tokyo and Niigata. Drugs and related agents tested were omeprazole, lansoprazole, rabeprazole, the thioether derivative of rabeprazole (rabeprazole-TH), clarithromycin, amoxicillin and metronidazole. The MICs of the drugs and agents for H. pylori strains were determined by the agar dilution method. Bacterial swimming in a liquid layer was examined under an inverted, phase-contrast microscope.〈section xml:id="abs1-4"〉〈title type="main"〉Results. The PPIs and rabeprazole-TH, but not the anti-H. pylori agents, inhibited the motility of CRHP at both pH 7.4 and 6.0. The concentrations (µg/ml) necessary to inhibit 50% of the motility at pH 7.4 were 0.25–0.5, 8–32, 8–16 and 128–256 for rabeprazole-TH, rabeprazole, lansoprazole and omeprazole, respectively. Rabeprazole-TH exibited the strongest inhibitory effect against the growth of CRPH (MIC, 0.5 µg/ml).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion. Rabeprazole-TH, which is secreted into the gastric mucosa, had the strongest inhibitory action against both the growth and motility of CRHP, suggesting that it is a potential novel agent for CRHP eradication.

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