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Helicobacter Pylori (helicobacter + pylori)
Kinds of Helicobacter Pylori Terms modified by Helicobacter Pylori Selected AbstractsINHIBITION OF HELICOBACTER PYLORI BY PHENOLIC EXTRACTS OF SPROUTED PEAS (PISUM SATIVUM L.)JOURNAL OF FOOD BIOCHEMISTRY, Issue 1 2006CHIA-YU HO ABSTRACT Infection by Helicobacter pylori is associated with gastric and duodenal ulcers. Conventional treatments to eradicate it have side-effects such as diarrhea and dizziness. The excessive use of antibiotics could also lead to antibiotic-resistant bacteria. The use of plant phenolic phytochemicals can be an alternative because of their health benefits due to both antioxidant activity and antimicrobial activity. The pea (Pisum sativum), the world's second most important pulse crop, produces phenolic phytochemicals with antimicrobial potential. Because the synthesis of phenolic compounds increases with stress, we investigated the anti- H. pylori effectiveness of extracts from pea sprouts, germinated in the dark condition following treatment with either distilled water or acetyl salicylic acid. The peas were germinated for 8 days and the sprouted samples were measured for total soluble phenolic content, antioxidant and guaiacol peroxidase activity. Subsequently, the sprout extracts were tested for anti- H. pylori activity using the agar diffusion method and the effective dose was determined based on phenolic content. The results showed that both acetyl salicylic acid-treated and untreated pea sprouts at days 5 and 8 had anti- H. pylori activity. The minimum volume for inhibition was 50 ,L of extracts. The inhibitory effects were dose dependent. From this study, the potential to use natural phenolic phytochemicals from pea sprouts to control H. pylori was found to be promising. This provides a strategy and foundation to design legume phenolics as functional ingredients against H. pylori. [source] Helicobacter Pylori and Precancerous Gastric LesionsDIGESTIVE ENDOSCOPY, Issue 3 2000Pham Quang Cu Background: To determine the relationship between Helicobacter pylori (H. pylori) infection and the precancerous gastric lesions: atrophic gastritis (AG) and intestinal metaplasia (IM) and dysplasia. Methods: A total of 347 dyspeptic patients, including 141 H. pylori -positive patients and 206 H. pylori -negative patients, were studied alongside age- and sex-matched controls. The patients underwent gastroscopy and endoscopic biopsy for detection of H. pylori, and histological examinations. Helicobacter pylori was detected by a urease test (CLO; Delta West; Bentley, Australia), by histology (H&E stain, Giemsa) and by serology (BioSig; BioMeditech, NJ, USA). Atrophic gastritis, IM and dysplasia were detected by histological examination (Giemsa, H&E stain). Results: There is a higher rate of atrophic gastritis in H. pylori -positive than in H. pylori -negative patients (46 vs 13.5%, odds ratio (OR) = 5.4; P < 0.01). Gastritis in H. pylori -positive patients also has a higher rate of activity than in H. pylori -negative patients. The rate of IM is higher in H. pylori -positive patients than in H. pylori -negative patients (35 vs 11%; OR = 4.3; P < 0.01). Metaplasia is more often diffuse in H. pylori -positive than in H. pylori -negative patients. Dysplasia is more common in H. pylori -positive than in H. pylori -negative patients (12 and 3.8%; OR = 3.3; P < 0.01). Conclusions: This study supports the suggestion of a relationship between H. pylori infection and precancerous gastric lesions. Wherever H. pylori is present, the precancerous lesions are more common and more severe. [source] Antagonistic Activity of Spent Culture Supernatants of Lactic Acid Bacteria against,Helicobacter Pylori,Growth and Infection in Human Gastric Epithelial AGS CellsJOURNAL OF FOOD SCIENCE, Issue 6 2009Wen-Hsin Lin ABSTRACT:, We investigated the bactericidal activity and exclusion effect of 10 strains of lactic acid bacteria (LAB) isolated from different commercial food products and infant feces against,Helicobacter pylori,(H. pylori) in human gastric epithelial AGS cells. Antagonistic activity of spent culture supernatants (SCS) from LAB (LAB-SCS) was tested, and the content of organic acids in SCS was analyzed with high-performance liquid chromatography (HPLC). In addition, the bactericidal activities of LAB-SCS were estimated by a time-kill assay and by measuring the exclusion effect of LAB-SCS against,H. pylori,in AGS cells. The results showed that SCS from certain strains with higher concentrations of organic acids dramatically decreased the viability of,H. pylori. We also proved that the organic acids could inhibit,H. pylori,adhesion and invasion of AGS cells. Furthermore, the concentration and speciation of organic acids in SCS after fermentation of LAB are important factors in the inhibition of,H. pylori,infection. In addition, the,in vitro,methods used in this study might provide for the rapid screening of potential probiotics with anti- H. pylori,activity in the dairy industry. [source] Reversible Cerebellar Lesions Induced by Metronidazole Therapy for Helicobacter PyloriJOURNAL OF NEUROIMAGING, Issue 4 2004Hirono Ito MD ABSTRACT Metronidazole is widely used for chronic or refractory infection and has recently also been used for the treatment of Helicobacter pylori. The authors report the case of a Japanese patient presenting with reversible cerebellar lesions induced by prolonged administration of metronidazole for treatment of H pylori with magnetic resonance imaging findings. Although rare, prolonged and high-dose administration of metronidazole may induce cerebellar lesions. Increased awareness of this phenomenon is important, as these lesions are reversible with discontinuation of this drug. [source] Current concepts in the management of Helicobacter pylori infection,The Maastricht 2-2000 Consensus ReportALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2002P. Malfertheiner Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21,22 September 2000. A ,test and treat' approach is recommended in adult patients under the age of 45 years (the age cut-off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro-oesophageal reflux disease symptoms, non-steroidal anti-inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test. As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low-grade gastric mucosa-associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first-degree relatives of gastric cancer patients and according to patients' wishes after full consultation. It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long-term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro-oesophageal reflux disease in most cases, and does not exacerbate existing gastro-oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non-steroidal anti-inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non-steroidal anti-inflammatory drugs. Treatment should be thought of as a package which considers first- and second-line eradication therapies together. First-line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second-line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second-line therapy should be with proton pump inhibitor-based triple therapy. If second-line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case-by-case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradica- tion should always be confirmed by urea breath test or an endoscopy-based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available. [source] Optimization of Allium sativum Solvent Extraction for the Inhibition of in Vitro Growth of Helicobacter PyloriBIOTECHNOLOGY PROGRESS, Issue 6 2002Pablo Cańizares Helicobacter pylori (Hp) is the bacterium responsible for serious gastric diseases such as ulcers and cancer. The work described here involved the study of the inhibitory power of Allium sativum extracts against the in vitro growth of Hp(Hp ivg). We used purple garlic of the "Las Pedrońeras" variety for this study. The effects of two different extraction methods (Soxhlet, stirred tank extractor) and four solvents with different characteristics (water, acetone, ethanol, and hexane) were investigated in terms of the efficiency of the extraction process. Satisfactory results were obtained in most cases in the activity tests, indicating that different extracts gave rise to good inhibitory activity against Hp ivg. The extracts that showed the highest bacteriostatic activities were selected to evaluate the influence of the most important operation variables on the extraction yield: stirring speed, operation time, garlic conditioning, and garlic storage time. The best results were obtained using ethanol and acetone as solvents in a stirred tank. The inhibitory powers of these extracts were compared to those shown by some commercial antibiotics used in the medical treatment of Hp infections. The results of this study show that garlic extracts produce levels of inhibition similar to those of the commercial materials. These extracts were also tested against other common bacteria, and equally satisfactory results were obtained. The research described here represents an important starting point in the fight against and/or prevention of peptic ulcers, as well as other pathologies associated with Hp infections such us gastric cancer. The extracted material can be used by direct application and involves a simple and economical extraction procedure that avoids isolation or purification techniques. [source] Helicobacter pylori activates protein kinase C delta to control Raf in MAP kinase signalling: Role in AGS epithelial cell scattering and elongationCYTOSKELETON, Issue 10 2009Sabine Brandt Abstract Helicobacter pylori is a major etiological agent in the development of chronic gastritis, duodenal ulcer and gastric carcinoma in humans. Virulent H. pylori strains harbor a type IV secretion system (T4SS) encoded by the cag pathogenicity island. This T4SS injects the CagA protein into gastric epithelial cells leading to actin-cytoskeletal rearrangements followed by cell elongation and scattering. Here we report that PMA (4,-phorbol-12-myristate-13-acetate), a well-known cell-permeable activator of protein kinase C (PKC), induces a remarkably similar cellular phenotype as compared to infection with H. pylori. PKCs comprise a large family of serine/threonine kinases which are important for multiple physiological processes of host cells. We therefore investigated the role of individual PKC members and the signalling pathways involved in phenotypical outcome. Using isoform-specific silencing RNAs and pharmacological inhibitors we found that two isoforms, PKC-, and PKC-,, were essential for both PMA- and H. pylori -induced elongation phenotype. Furthermore, we provide evidence that PKC-, activity is profoundly stimulated during the course of infection using activation-specific antibodies against PKC phosphorylated at threonine residue 505 or serine residue 660. Infection with H. pylori wild-type and mutants showed that at least two bacterial factors activate PKC-, in a time-dependent manner, one of which is CagA. Immunofluorescence microscopy studies further demonstrated that phosphorylated PKC-, is accumulated and recruited to dynamic actin-structures at the cell membrane. Finally, we show that PKC-, specifically targets Raf kinase to stimulate the Erk1/2 kinase pathway, which is also crucial for phenotypical outcome. Thus, PKC-, is another important mediator of H. pylori -induced pathogenesis. Cell Motil. Cytoskeleton 2009. © 2009 Wiley-Liss, Inc. [source] PARTIAL REGRESSION OF DUODENAL LESIONS OF INTESTINAL FOLLICULAR LYMPHOMA AFTER ANTIBIOTIC TREATMENTDIGESTIVE ENDOSCOPY, Issue 4 2010Tomonori Yaguchi A 51-year-old man was referred to our hospital because of duodenal lesions of lymphoma. Endoscopy showed multiple tiny smooth whitish granules in the second portion of the duodenum including the papilla of Vater. Biopsy specimens showed medium-sized centrocyte-like cells forming lymphoid follicles, and immunohistology showed positive staining for bcl-2 and CD10. A small bowel series showed multiple granular lesions extending from the second portion of the duodenum to the proximal jejunum and the proximal ileum. On the basis of these findings, the tumor was diagnosed as stage I follicular lymphoma (FL). Although the patient was negative for Helicobacter pylori, he underwent antibiotic treatment. The lesions improved 3 months after antibiotic treatment, but biopsy specimens showed residual lymphoma cells. The patient therefore received combination chemotherapy with rituximab. Endoscopy 4 months later showed regression of FL, and there was no evidence of recurrence during 3 years of follow up. The partial regression of duodenal lesions of intestinal FL may be due to the effect of antibiotic treatment. [source] ENDOSCOPIC IDENTIFICATION OF HELICOBACTER PYLORI GASTRITIS IN CHILDRENDIGESTIVE ENDOSCOPY, Issue 2 2010Nao Hidaka Aim:, The role of endoscopic findings in deciding whether to biopsy the gastric mucosa of children remains unclear. The present study attempted, for the first time, to identify the value of endoscopic features for diagnosis of Helicobacter pylori (Hp) infection in children. Methods:, Hp status of consecutive children receiving esophagogastroduodenoscopy (EGD) was established by combinations of histology, 13C-urea breath test, and serum Hp immunoglobulin (Ig)G antibody. After routine EGD using a conventional endoscope, the presence of RAC (regular arrangement of collecting venules) was scored by close observation, which was carried out at two sites of lower corpus lesser curvature and upper corpus greater curvature. RAC-positive was defined as the presence of minute red points in a regular pattern. Antral nodularity was also scored as present/absent. Results:, Eighty-seven consecutive children (38 boys, median age 13 years, range 9,15 years) were evaluated; 25 (29%) were Hp positive. Antral nodularity was seen in 21 (84%) all of whom were Hp positive. The RAC-negative pattern based on examination of the upper and lower corpus yielded a sensitivity, specificity, positive predictive value and negative predictive value for the presence of Hp infection of 100%, 90%, 81%, and 100%. Magnifying endoscopy confirmed that the RAC pattern corresponded to collecting venules in the gastric corpus. Conclusions:, The absence of RAC pattern suggests that gastric mucosa biopsies should be taken despite otherwise normal-appearing gastric mucosa for the diagnosis of Hp infection in children. [source] PREDICTIVE VALUE OF ENDOSCOPY AND ENDOSCOPIC ULTRASONOGRAPHY FOR REGRESSION OF GASTRIC DIFFUSE LARGE B-CELL LYMPHOMAS AFTER HELICOBACTER PYLORI ERADICATIONDIGESTIVE ENDOSCOPY, Issue 4 2009Akira Tari Background:, Some gastric diffuse large B-cell lymphomas have been reported to regress completely after the successful eradication of Helicobacter pylori. The aim of this study was to investigate the clinical characteristics of gastric diffuse large B-cell lymphomas without any detectable mucosa-associated lymphoid tissue (MALT) lymphoma that went into complete remission after successful H. pylori eradication. Patients and Methods:, We examined the effect of H. pylori eradication in 15 H. pylori -positive gastric diffuse large B-cell lymphoma patients without any evidence of an associated MALT lymphoma (clinical stage I by the Lugano classification) by endoscopic examination including biopsies, endoscopic ultrasonography, computed tomography, and bone marrow aspiration. Results:,H. pylori eradication was successful in all the patients and complete remission was achieved in four patients whose clinical stage was I. By endoscopic examination, these gastric lesions appeared to be superficial. The depth by endoscopic ultrasonography was restricted to the mucosa in two patients and to the shallow portion of the submucosa in the other two patients. All four patients remained in complete remission for 7,100 months. Conclusion:, In gastric diffuse large B-cell lymphomas without a concomitant MALT lymphoma but associated with H. pylori infection, only superficial cases and lesions limited to the shallow portion of the submucosa regressed completely after successful H. pylori eradication. The endoscopic appearance and the rating of the depth of invasion by endosonography are both valuable for predicting the efficacy of H. pylori eradication in treating gastric diffuse large B-cell lymphomas. [source] ENDOSCOPIC MICROVASCULAR ARCHITECTURE OF THE PORTAL HYPERTENSIVE GASTRIC MUCOSA ON NARROW BAND IMAGINGDIGESTIVE ENDOSCOPY, Issue 3 2007Seishu Hayashi Background:, We evaluated the endoscopic microvascular architecture of the gastric mucosa in portal hypertension patients using the prototype of narrow band imaging (NBI). Material and Methods:, The study included 103 Helicobacter pylori -negative patients with chronic liver disease (22 without portal hypertension (group 1), 81 with portal hypertension (group 2)). Results:, (i) Abnormality of collecting venules, reddening mucosa, red spots, a mosaic-like pattern, and gastric antral vascular ectasia (GAVE) were observed on the gastric mucosa, and an obscure change in collecting venules (73% vs 14%; P < 0.001), reddening mucosa (49% vs 5%; P < 0.001), red spots (36% vs 5%; P < 0.01) and a mosaic-like pattern (40% vs 5%; P < 0.01) were more frequently observed in group 2 than in group 1. (ii) On magnifying endoscopy with NBI, the mucosa with an obscure change in collecting venules was demonstrated as dilation of the capillaries surrounding the gastric pits in various degrees, and reddening mucosa was observed as extended and swollen gastric pits and various degrees of dilated and convoluted capillaries surrounding the gastric pits. Red spots were demonstrated as extended and swollen gastric pits, dilated and convoluted capillaries surrounding the gastric pits, and intramucosal hemorrhage around these capillaries. GAVE was recognized as partial and marked dilatation of the capillaries surrounding the gastric pits. Conclusion:, Abnormality of collecting venules, swelling of gastric pits, dilatation of capillaries surrounding the gastric pits, intramucosal hemorrhage around capillaries, and partial and marked dilatation of the capillaries were observed on the gastric mucosa in portal hypertension patients. [source] SMALL EARLY GASTRIC CANCER OCCURRING IN A YOUNG WOMAN WITH NODULAR GASTRITISDIGESTIVE ENDOSCOPY, Issue 2 2007Shuji Kochi We found a small gastric cancer in a 25-year-old woman with nodular gastritis. Endoscopically, the cancer was identified as a whitish area in the gastric antrum. There was also a miliary pattern in the gastric antrum and corpus. In addition, serology and histology revealed the patient to have been infected by Helicobacter pylori. Histological examination of the resected stomach showed that the cancer was poorly differentiated adenocarcinoma with signet-ring cell restricted to the mucosal layer. In the surrounding mucosa, there were chronic inflammatory cell infiltrates and enlarged lymphoid follicles with germinal centers. Our case suggests that nodular gastritis may be at a high risk for the development of gastric cancer of poorly differentiated type. [source] NODULAR GASTRITIS AND GASTRIC CANCERDIGESTIVE ENDOSCOPY, Issue 2 2006Tomoari Kamada Nodular gastritis is defined as antral gastritis usually characterized endoscopically by a miliary pattern resembling gooseflesh and pathologically by prominent lymphoid follicles and infiltration of mononuclear cells. This physiological phenomenon was once considered particular to young women. Recent studies have shown that nodular gastritis is strongly associated with Helicobacter pylori infection and may be associated with gastric cancer. Reported cases of gastric cancer with nodular gastritis showed some features in common: all gastric cancers were diagnosed histologically as the diffuse-type, and all were located in the corpus with Helicobacter pylori infection. Because nodular gastritis may be a risk factor for diffuse-type gastric cancer, Helicobacter pylori may need to be eradicated to prevent gastric cancer in patients with nodular gastritis. [source] RECENT PROGRESS IN ENDOSCOPY-BASED DIAGNOSIS OF HELICOBACTER PYLORI INFECTIONDIGESTIVE ENDOSCOPY, Issue 1 2001Tadashi Sato Numerous invasive and non-invasive tests are available in the detection of Helicobacter pylori. Endoscopy-based tests that include rapid urease test, histological examination and culture are important generally in the assessment of H. pylori status before eradication therapy. Recently, several new endoscopy-based diagnostic methods have been developed aiming at rapid and accurate detection of the organisms. It would be possible to diagnose H. pylori infection in treated patients by using these new highly sensitive tests. Although the diagnosis of H. pylori infection itself is possible by using non-invasive diagnostic tests, endoscopy-based tests provide not only the diagnosis of the organisms, but also the exclusive information such as treatment indications and the susceptibility for the antimicrobial drugs. Recently, new triple therapy including clarithromycin has been widely performed in Japan. Along with an increase in the prevalence of the antibiotic-resistant strains, culture may become a more important diagnostic method in the future. The inappropriate application of the tests may increase the potential risk of the misdiagnosis and the treatment failures. The diagnostic method should be selected by taking into account the circumstances in which a diagnosis is to be performed. [source] Helicobacter Pylori and Precancerous Gastric LesionsDIGESTIVE ENDOSCOPY, Issue 3 2000Pham Quang Cu Background: To determine the relationship between Helicobacter pylori (H. pylori) infection and the precancerous gastric lesions: atrophic gastritis (AG) and intestinal metaplasia (IM) and dysplasia. Methods: A total of 347 dyspeptic patients, including 141 H. pylori -positive patients and 206 H. pylori -negative patients, were studied alongside age- and sex-matched controls. The patients underwent gastroscopy and endoscopic biopsy for detection of H. pylori, and histological examinations. Helicobacter pylori was detected by a urease test (CLO; Delta West; Bentley, Australia), by histology (H&E stain, Giemsa) and by serology (BioSig; BioMeditech, NJ, USA). Atrophic gastritis, IM and dysplasia were detected by histological examination (Giemsa, H&E stain). Results: There is a higher rate of atrophic gastritis in H. pylori -positive than in H. pylori -negative patients (46 vs 13.5%, odds ratio (OR) = 5.4; P < 0.01). Gastritis in H. pylori -positive patients also has a higher rate of activity than in H. pylori -negative patients. The rate of IM is higher in H. pylori -positive patients than in H. pylori -negative patients (35 vs 11%; OR = 4.3; P < 0.01). Metaplasia is more often diffuse in H. pylori -positive than in H. pylori -negative patients. Dysplasia is more common in H. pylori -positive than in H. pylori -negative patients (12 and 3.8%; OR = 3.3; P < 0.01). Conclusions: This study supports the suggestion of a relationship between H. pylori infection and precancerous gastric lesions. Wherever H. pylori is present, the precancerous lesions are more common and more severe. [source] Gastroesophageal reflux before and after Helicobacter pylori eradication.DISEASES OF THE ESOPHAGUS, Issue 4 2003A prospective study using ambulatory 24-h esophageal pH monitoring SUMMARY, The aim of this study was to assess prevalence of GERD before and after Helicobacter pylori (HP) eradication utilizing 24-h esophageal pH/manometry studies. Helicobacter pylori status was confirmed by the Campylobacter like organism test. Those testing positive underwent 24-h pH/manometry followed by HP eradication therapy and urea breath test. Patients were followed up at 6 months and then at 1 year when they underwent a repeat 24-h pH/manometry. Twenty patients, 10 with non-ulcer dyspepsia (NUD) and 10 with duodenal ulcer (DU) were enrolled, though only 10 patients attended for a repeat 24-h pH/manometry study. The patients were well matched, though patients with NUD had a significantly higher symptom score at entry compared with the DU group (8.5 vs 5.7, P < 0.05). The pH and esophageal manometry data were similar in the two groups. Overall nine patients (45%; DU = 5, NUD = 4) had evidence of GERD prior to HP eradication and it persisted one year after cure of the infection. The reflux disease occurred in the presence of normal LES pressure (mean 15.6 ± 3.3 mmHg). New onset GERD was uncommon after cure of HP infection, occurring in only one patient with NUD. Overall HP eradication had no impact on percentage of time pH < 4 (4.69 ± 3 vs 4.79 ± 3), episodes > 5 min (9.8 ± 16 vs 15.5 ± 25.3) and Johnson DeMeester Score (16.8 ± 7.5 vs 26.8 ± 18). In addition successful cure of HP produced no significant changes in LES pressure (17.9 ± 3.8 mmHg vs 19.3 ± 4.6 mmHg), and other esophageal manometry data. Half of HP-positive patients with NUD and DU have evidence of GERD before HP eradication. This persists after successful cure of the infection. New onset GERD occurs very uncommonly one year after HP eradication. [source] Fundal gastritis as a potential cause of reflux oesophagitisDISEASES OF THE ESOPHAGUS, Issue 1 2000M. Newton The transient lower oesophageal sphincter relaxations which allow reflux may be due to altered afferent pathways from the fundus. We aimed to determine whether fundal inflammation is the underlying cause. Two endoscopic biopsies were taken from each of the gastric antrum and fundus in 25 asymptomatic controls with a normal endoscopy (median age 54 range 13,83 years), and 33 patients with erosive oesophagitis (median age 52, 11,78 years). No patient had taken acid suppression therapy or antibiotics for at least 1 month. Sections were stained with haematoxylin and eosin and Giemsa stain and examined in a blinded fashion by one pathologist for the presence of gastritis (Sydney classification) and Helicobacter pylori. Chronic gastritis was common in both groups, but was usually mild. In Helicobacter pylori -negative subjects, there was significantly less chronic gastritis in the antrum and the fundus in oesophagitis patients than in controls (p < 0.05). When present, gastric atrophy was usually antral and mild in severity. There was no difference in the incidence of gastric atrophy in patients with oesophagitis compared with controls (24% compared with 40%; p > 0.05). Chronic gastritis is not more common in patients with oesophagitis, and is unlikely to play a part in the pathogenesis of this disease. [source] Growth-induced changes in the proteome of Helicobacter pyloriELECTROPHORESIS, Issue 5-6 2006Christina Uwins Abstract Helicobacter pylori is a major human pathogen that is responsible for a number of gastrointestinal infections. We have used 2-DE to characterise protein synthesis in bacteria grown either on solid agar-based media or in each of two broth culture media (Brucella and brain heart infusion (BHI) broth). Significant differences were observed in the proteomes of bacteria grown either on agar-based or in broth media. Major changes in protein abundance were identified using principal component analysis (PCA), which delineated the profiles derived for the three key growth conditions (i.e. agar plates, Brucella and BHI broth). Proteins detected across the gel series were identified by peptide mass mapping and Edman sequencing. A number of proteins associated with protein synthesis in general as well as specific amino acid synthesis were depressed in broth-grown bacteria compared to plate-grown bacteria. A similar reduction was also observed in the abundance of proteins involved in detoxification. Two of the most abundant spots, identified as UreB and GroEL, in plate-grown bacteria showed a >140-fold drop in abundance in bacteria grown in Brucella broth compared to bacteria grown on agar plates. Two protein spots induced in bacteria grown in broth culture were both identified as glyceraldehyde 3-phosphate dehydrogenase based on their N -terminal amino acid sequences derived by Edman degradation. The underlying causes of the changes in the proteins abundance were not clear, but it was likely that a significant proportion of the changes were due to the alkaline pH of the broth culture media. [source] Relationships between cagA, vacA, and iceA genotypes of Helicobacter pylori and DNA damage in the gastric mucosaENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2004Marcelo S.P. Ladeira Abstract Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage in the gastric mucosa and cagA, vacA, and iceA genotypes of H. pylori. The study was conducted with biopsies from the gastric antrum and corpus of 98 H. pylori -infected and 26 uninfected control patients. H. pylori genotypes were determined by PCR and DNA damage was measured in gastric mucosal cells by the Comet assay (single cell gel electrophoresis). All patients were nonsmokers, not abusing alcohol, and not using prescription or recreational drugs. Levels of DNA damage were significantly higher (P < 0.0001) in the H. pylori -infected patients than in uninfected patients. In comparison with the level of DNA damage in the uninfected controls, the extent of DNA damage in both the antrum (OR = 8.45; 95% CI = 2.33,37.72) and the corpus (OR = 6.55; 95% CI = 2.52,17.72) was related to infection by cagA+/vacAs1m1 and iceA1 strains. The results indicate that the genotype of H. pylori is related to the amount of DNA damage in the gastric mucosa. These genotypes could serve as biomarkers for the risk of extensive DNA damage and possibly gastric cancer. Environ. Mol. Mutagen. 44:91,98, 2004. © 2004 Wiley-Liss, Inc. [source] Comparative study on antibodies to human and bacterial 60 kDa heat shock proteins in a large cohort of patients with coronary heart disease and healthy subjectsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2001Z. Prohászka Background Recent observations indicate an association between antibodies against mycobacterial heat shock protein (hsp65) and coronary heart disease (CHD). Previously, we reported on marked differences in antigen specificity and complement activating ability of anti-hsp65 antibodies and auto-antibodies against human heat shock protein, hsp60. Here, we investigated whether there are differences between antih-sp65 and anti-hsp60 antibodies in their association with CHD. Design We measured by ELISA the levels of antibodies to hsp65, hsp60 and E. coli -derived GroEL in three groups: Group I, 357 patients with severe CHD who underwent by-pass surgery; Group II, 67 patients with negative coronary angiography; Group III, 321 healthy blood donors. Antibodies against Helicobacter pylori were also measured by commercial ELISA. Results As calculated by multiple regression analysis, the levels of anti-hsp60 auto-antibodies were significantly higher in Group I compared to Group II (P = 0·007) or Group III (P < 0·0001). By contrast, although concentrations of anti-hsp65 and anti-GroEL antibodies in Group I were higher than in Group III, no significant differences between Group I and Group II were found. Antibodies to the two bacterial hsp strongly correlated to each other, but either did not correlate or weakly correlated to hsp60. In Group I, serum concentrations of anti- H.pylori antibodies significantly correlated with those of anti-hsp65 and anti-GroEL antibodies but they did not correlate with the anti-hsp60 antibodies. Conclusion As to their clinical relevance, a remarkable difference become evident between antibodies to human hsp60 and antibodies against bacterial hsp in the extent of association with CHD. On the basis of these findings and some pertinent literature data, an alternative explanation for the association between high level of anti-hsp antibodies and atherosclerotic vascular diseases is raised. [source] HIV+ MALT lymphoma remission induced by highly active antiretroviral therapy aloneEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 1 2005Thomas Girard Abstract:, MALT lymphoma is usually described in association with Helicobacter pylori, HCV, HHV8, Campylobacter jejuni or in a setting of overreactive immunity. In HIV+ patients, MALT lymphoma is most commonly described in children. We describe here an original case of HIV+ MALT lymphoma with bronchial, conjuctival and laryngeal involvement for which a clinical and histopathological remission has been obtained with HAART alone. We conclude that HIV, as well as H. pylori, C. jejuni and HCV can target lymphogenesis in MALT lymphoma. [source] Prevention of cancer through immunization: Prospects and challenges for the 21st centuryEUROPEAN JOURNAL OF IMMUNOLOGY, Issue S1 2007Abstract Persistent infection by several microbial agents is responsible for at least 15% of cancer globally, including most cancers of the liver, stomach, and cervix. The recent development of vaccines that can prevent infection and premalignant disease caused by human papillomaviruses (HPV), which cause virtually all cases of cervical cancer as well as some other cancers, has focused renewed attention on infection control as a means of reducing the global cancer burden. For vaccines to prevent cancer-causing infection with hepatitis C virus, Helicobacter pylori, or Epstein Barr virus, new vaccine technologies to induce more effective protective responses are required. For the two available cancer control vaccines, designed to prevent infection with HPV and hepatitis B virus, the major challenge is to promote effective vaccine deployment through education programs and increased affordability/accessibility for underserved populations, particularly in the developing world, where the cancer burden attributable to infection by these two viruses is greatest. [source] Helicobacter pylori in human oral cavity and stomachEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 4 2008Ralf Bürgers The oral cavity has been suspected as an extra-gastroduodenal reservoir for Helicobacter pylori infection and transmission, but conflicting evidence exists regarding the occurrence of H. pylori in the mouth, independently of stomach colonization. Ninety-four gastric biopsy patients were analysed for the concurrent presence of H. pylori in the mouth and stomach. Samples were collected from different areas within the mouth and H. pylori DNA was amplified by the polymerase chain reaction (PCR) and verified by sequencing. Helicobacter pylori -specific serology was performed, and stomach colonization was determined by culture. In addition, relevant dental and periodontal parameters, as well as general health parameters, were recorded. Helicobacter pylori was found in the stomach of 29 patients and in the oral cavity of 16 patients. In only six patients was the bacterium detected simultaneously in the stomach and mouth. Notably, the 10 patients in whom the bacterium was found solely in the mouth did not have serum antibodies to H. pylori. The occurrence of H. pylori in the mouth was found to be correlated neither to any general or oral health parameters, nor to any particular site of collection. This study shows that H. pylori can occur in the oral cavity independently of stomach colonization. [source] Structural and mutational analysis of TenA protein (HP1287) from the Helicobacter pylori thiamin salvage pathway , evidence of a different substrate specificityFEBS JOURNAL, Issue 21 2009Nicola Barison HP1287 (tenA) from Helicobacter pylori is included among the genes that play a relevant role in bacterium colonization and persistence. The gene has been cloned and its product, protein TenA, has been expressed and purified. The crystal structures of the wild-type protein and the mutant F47Y have been determined at resolutions of 2.7 and 2.4 Ĺ, respectively. The molecular model, a homotetramer with 222 symmetry, shows that the H. pylori TenA structure belongs to the thiaminase II class of proteins. These enzymes were recently found to be involved in a salvage pathway for the synthesis of the thiamin precursor hydroxypyrimidine, which constitutes a building block in thiamin biosynthesis, in particular in bacteria living in the soil. By contrast, enzymatic measurements on TenA from H. pylori indicate that the activity on the putative substrate 4-amino-5-aminomethyl-2-methylpyrimidine is very modest. Moreover, in the present study, we demonstrate that the mutation at residue 47, a position where a phenylalanine occurs in all the strains of H. pylori sequenced to date, is not sufficient to explain the very low catalytic activity toward the expected substrate. As a result of differences in the colonization environment of H. pylori as well as the TenA structural and catalytic peculiar features, we suggest a possible pivotal role for the H. pylori enzyme in the thiamin biosynthetic route, which is in agreement with the relevance of this protein in the stomach colonization process. Structured digital abstract ,,MINT-7260232: TenA (uniprotkb:O25874) and TenA (uniprotkb:O25874) bind (MI:0407) by x-ray crystallography (MI:0114) [source] Biochemical characterization and inhibitor discovery of shikimate dehydrogenase from Helicobacter pyloriFEBS JOURNAL, Issue 20 2006Cong Han Shikimate dehydrogenase (SDH) is the fourth enzyme involved in the shikimate pathway. It catalyzes the NADPH-dependent reduction of 3-dehydroshikimate to shikimate, and has been developed as a promising target for the discovery of antimicrobial agent. In this report, we identified a new aroE gene encoding SDH from Helicobacter pylori strain SS1. The recombinant H. pylori shikimate dehydrogenase (HpSDH) was cloned, expressed, and purified in Escherichia coli system. The enzymatic characterization of HpSDH demonstrates its activity with kcat of 7.7 s,1 and Km of 0.148 mm toward shikimate, kcat of 7.1 s,1 and Km of 0.182 mm toward NADP, kcat of 5.2 s,1 and Km of 2.9 mm toward NAD. The optimum pH of the enzyme activity is between 8.0 and 9.0, and the optimum temperature is around 60 °C. Using high throughput screening against our laboratory chemical library, five compounds, curcumin (1), 3-(2-naphthyloxy)-4-oxo-2-(trifluoromethyl)-4H -chromen-7-yl 3-chlorobenzoate (2), butyl 2-{[3-(2-naphthyloxy)-4-oxo-2-(trifluoromethyl)-4H -chromen-7-yl]oxy}propanoate (3), 2-({2-[(2-{[2-(2,3-dimethylanilino)-2-oxoethyl]sulfanyl}-1,3-benzothiazol-6-yl)amino]-2-oxoethyl}sulfanyl)- N -(2-naphthyl)acetamide (4), and maesaquinone diacetate (5) were discovered as HpSDH inhibitors with IC50 values of 15.4, 3.9, 13.4, 2.9, and 3.5 µm, respectively. Further investigation indicates that compounds 1, 2, 3, and 5 demonstrate noncompetitive inhibition pattern, and compound 4 displays competitive inhibition pattern with respect to shikimate. Compounds 1, 4, and 5 display noncompetitive inhibition mode, and compounds 2 and 3 show competitive inhibition mode with respect to NADP. Antibacterial assays demonstrate that compounds 1, 2, and 5 can inhibit the growth of H. pylori with MIC of 16, 16, and 32 µg·mL,1, respectively. This current work is expected to favor better understanding the features of SDH and provide useful information for the development of novel antibiotics to treat H. pylori -associated infection. [source] Characterization of cinnamyl alcohol dehydrogenase of Helicobacter pyloriFEBS JOURNAL, Issue 5 2005An aldehyde dismutating enzyme Cinnamyl alcohol dehydrogenases (CAD; 1.1.1.195) catalyse the reversible conversion of p -hydroxycinnamaldehydes to their corresponding alcohols, leading to the biosynthesis of lignin in plants. Outside of plants their role is less defined. The gene for cinnamyl alcohol dehydrogenase from Helicobacter pylori (HpCAD) was cloned in Escherichia coli and the recombinant enzyme characterized for substrate specificity. The enzyme is a monomer of 42.5 kDa found predominantly in the cytosol of the bacterium. It is specific for NADP(H) as cofactor and has a broad substrate specificity for alcohol and aldehyde substrates. Its substrate specificity is similar to the well-characterized plant enzymes. High substrate inhibition was observed and a mechanism of competitive inhibition proposed. The enzyme was found to be capable of catalysing the dismutation of benzaldehyde to benzyl alcohol and benzoic acid. This dismutation reaction has not been shown previously for this class of alcohol dehydrogenase and provides the bacterium with a means of reducing aldehyde concentration within the cell. [source] Oral vaccination of mice against Helicobacter pylori with recombinant Lactococcus lactis expressing urease subunit BFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2009Qing Gu Abstract To determine whether a protective immune response could be elicited by oral delivery of a recombinant live bacterial vaccine, Helicobacter pylori urease subunit B (UreB) was expressed for extracellular expression in food-grade bacterium Lactococcus lactis. The UreB-producing strains were then administered orally to mice, and the immune response to UreB was examined. Orally vaccinated mice produced a significant UreB-specific serum immunoglobulin G (IgG) response. Specific anti-UreB IgA responses could be detected in the feces of mice immunized with the secreting lactococcal strain. Mice vaccinated orally were significantly protected against gastric Helicobacter infection following a challenge with H. pylori strain SS1. In conclusion, mucosal vaccination with L. lactis expressing UreB produced serum IgG and UreB-specific fecal IgA, and prevented gastric infection with H. pylori. [source] Helicobacter pylori, coccoid forms and biofilm formationFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2009Leif Percival Andersen Abstract Electron microscopic studies have shown that Helicobacter pylori occurs in three stages: spiral forms, coccoid forms and degenerative forms. The spiral forms are viable, culturable, virulent and can colonize experimental animals and induce inflammation. The coccoid forms may also be viable but are nonculturable, less virulent and are less likely to colonize and induce inflammation in experimental animals than the spiral forms. The degenerative forms are pyknotic, nonculturable, coccoid forms of dead H. pylori. These forms cannot be cultured and the cell membrane has disintegrated but gene material can be detected by PCR in water supplies. There is no substantial evidence for viable H. pylori persisting in water supplies. Epidemiological studies suggest that environmental water is a risk factor for H. pylori infection when compared with tap water, and formation of H. pylori biofilm cannot be excluded. Helicobacter pylori does not seem to take part in biofilm formation in the oral cavity even though the bacterium may be detected. [source] The role of genome diversity and immune evasion in persistent infection with Helicobacter pyloriFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2005Cara L. Cooke Abstract Helicobacter pylori is an important human pathogen that chronically colonizes the stomach of half the world's population. Infection typically occurs in childhood and persists for decades, if not for the lifetime of the host. How is bacterial persistence possible despite a vigorous innate and adaptive immune response? Here we describe the complex role of bacterial diversity and specific mechanisms to avoid or subvert host immunity in bacterial persistence. We suggest that H. pylori finely modulates the extent to which it interacts with the host in order to promote chronic infection, and that it uses diverse mechanisms to do so. [source] Identification of Helicobacter pylori and the cagA genotype in gastric biopsies using highly sensitive real-time PCR as a new diagnostic toolFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2005Shiho Yamazaki Abstract The CagA protein is one of the virulence factors of Helicobacter pylori, and two major subtypes of CagA have been observed, the Western and East Asian type. CagA is injected from the bacteria into gastric epithelial cells, undergoes tyrosine phosphorylation, and binds to Src homology 2 domain-containing protein-tyrosine phosphatase SHP-2. The East Asian type CagA binds to SHP-2 more strongly than the Western type CagA. Here, we tried to distinguish the CagA type by highly sensitive real-time PCR with the objective of establishing a system to detect H. pylori and CagA subtypes from gastric biopsies. We designed primers and probe sets for Western or East Asian- cagA at Western-specific or East Asian-specific sequence regions, respectively, and H. pylori 16S rRNA. We could detect the H. pylori 16S rRNA gene, Western and East Asian- cagA gene from DNA of gastric biopsies. The sensitivity and specificity for H. pylori infection was 100% in this system. In Thai patients, 87.8% (36/41) were cagA -positive; 26.8% (11/41) were Western- cagA positive and 53.7% (22/41) were East Asian- cagA positive, while 7.3% (3/41) reacted with both types of cagA. These results suggest that this real-time PCR system provides a highly sensitive assessment of CagA type as a new diagnostic tool for the pathogenicity of H. pylori infection. [source] | |||||||||||||||||||||||||||||||||||||