scholarly journals Evaluation of the AnaeroPack Campylo System for Growth of Microaerophilic Bacteria

1999 ◽  
Vol 37 (7) ◽  
pp. 2376-2377 ◽  
Author(s):  
Kenneth Van Horn ◽  
Clara Tóth
Keyword(s):  
New York ◽  
Helicobacter Pylori ◽  
Campylobacter Jejuni ◽  
Growth Control ◽  
Colony Morphology ◽  
Generation System ◽  
Becton Dickinson ◽  
H Pylori ◽  
Better Than

Growth of microaerophilic bacteria in the AnaeroPack Campylo (Mitsubishi Gas Chemical America, Inc., New York, N.Y.) atmosphere generation system was compared to growth in the CampyPak Plus jar and CampyPak pouch (Becton-Dickinson Microbiology Systems [BDMS], Cockeysville, Md.). Growth in the AnaeroPack Campylo system was considered equivalent to or better than growth obtained in the CampyPak Plus and CampyPak pouch systems for 48 of the 50 Helicobacter pylori strains and for all 28 Campylobacter species tested. All of the 78 organisms tested were recovered in each system in equivalent colony counts. Two strains of H. pylori grown in the AnaeroPack Campylo system were observed to have colony morphology growth discrepancies when compared to growth in the two BDMS systems. Atmosphere failure with the AnaeroPack Campylo was not detected withCampylobacter jejuni ATCC 33291 used as a growth control. The AnaeroPack Campylo system is easy to use and supports the growth of campylobacters and H. pylori.

scholarly journals Seroepidemiology ofHelicobacter pyloriinfection in vegans and meat-eaters

1992 ◽  
Vol 108 (3) ◽  
pp. 457-462 ◽  
Author(s):  
M. J. Webberley ◽  
J. M. Webberley ◽  
D. G. Newell ◽  
P. Lowe ◽  
V. Melikian
Keyword(s):  
Helicobacter Pylori ◽  
Risk Factor ◽  
Campylobacter Jejuni ◽  
Meat Consumption ◽  
Cross Reactivity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Igg Antibody ◽  
Specific Igg ◽  
H Pylori ◽  
Age And Sex

SUMMARYAn enzyme-linked immunosorbent assay has been used to diagnose serologically the prevalence ofHelicobacter pyloriinfection in Asian life-long vegans. There was no difference in the seropositivity between these individuals and a group of age-and sex-matched Asian meat-eaters, indicating the meat consumption is not a risk factor forH. pyloriinfection. However, both Asian groups had a higher prevalence of infection than age- and sex-matched Caucasian meat-eaters. Additionally, the Asian individuals had a wider range of specific IgG antibody concentrations than the Caucasians. This did not appear to be due to antigenic cross-reactivity betweenH. pyloriandCampylobacter jejuni. The significance of these observations to the establishment of cut-off levels for the serodiagnosis of certain ethnic groups is discussed.

scholarly journals Antiparasitic Drug Nitazoxanide Inhibits the Pyruvate Oxidoreductases of Helicobacter pylori, Selected Anaerobic Bacteria and Parasites, and Campylobacter jejuni

2006 ◽  
Vol 51 (3) ◽  
pp. 868-876 ◽  
Author(s):  
Paul S. Hoffman ◽  
Gary Sisson ◽  
Matthew A. Croxen ◽  
Kevin Welch ◽  
W. Dean Harman ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Campylobacter Jejuni ◽  
Trichomonas Vaginalis ◽  
Enzymatic Reaction ◽  
Anaerobic Bacteria ◽  
Spectral Shift ◽  
Thiamine Pyrophosphate ◽  
Escape Mutation ◽  
Thiazole Ring ◽  
H Pylori

ABSTRACT Nitazoxanide (NTZ) exhibits broad-spectrum activity against anaerobic bacteria and parasites and the ulcer-causing pathogen Helicobacter pylori. Here we show that NTZ is a noncompetitive inhibitor (Ki , 2 to 10 μM) of the pyruvate:ferredoxin/flavodoxin oxidoreductases (PFORs) of Trichomonas vaginalis, Entamoeba histolytica, Giardia intestinalis, Clostridium difficile, Clostridium perfringens, H. pylori, and Campylobacter jejuni and is weakly active against the pyruvate dehydrogenase of Escherichia coli. To further mechanistic studies, the PFOR operon of H. pylori was cloned and overexpressed in E. coli, and the multisubunit complex was purified by ion-exchange chromatography. Pyruvate-dependent PFOR activity with NTZ, as measured by a decrease in absorbance at 418 nm (spectral shift from 418 to 351 nm), unlike the reduction of viologen dyes, did not result in the accumulation of products (acetyl coenzyme A and CO2) and pyruvate was not consumed in the reaction. NTZ did not displace the thiamine pyrophosphate (TPP) cofactor of PFOR, and the 351-nm absorbing form of NTZ was inactive. Optical scans and 1H nuclear magnetic resonance analyses determined that the spectral shift (A 418 to A 351) of NTZ was due to protonation of the anion (NTZ−) of the 2-amino group of the thiazole ring which could be generated with the pure compound under acidic solutions (pKa = 6.18). We propose that NTZ− intercepts PFOR at an early step in the formation of the lactyl-TPP transition intermediate, resulting in the reversal of pyruvate binding prior to decarboxylation and in coordination with proton transfer to NTZ. Thus, NTZ might be the first example of an antimicrobial that targets the “activated cofactor” of an enzymatic reaction rather than its substrate or catalytic sites, a novel mechanism that may escape mutation-based drug resistance.

scholarly journals Detection of Helicobacter pylori in gastric biopsy and resection specimens

2005 ◽  
Vol 62 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Tatjana Babic ◽  
Hakija Basic ◽  
Biljana Selimovic-Miljkovic ◽  
Branislava Kocic ◽  
Gordana Tasic
Keyword(s):  
Duodenal Ulcer ◽  
Alkaline Phosphatase ◽  
Helicobacter Pylori ◽  
Gastric Biopsy ◽  
Giemsa Stain ◽  
Biopsy Specimens ◽  
H Pylori ◽  
Antral Biopsy ◽  
Better Than ◽  
Immunohistochemical Identification

Aim. To compare the sensitivity of detecting H. pylori in gastric biopsy and resection specimens using modified Giemsa stain and immunohistochemistry, using a commercially available anti-H. pylori antibody (Dako, Denmark). Methods. Gastric antral biopsy specimens showing chronic gastritis (28 cases) together with tissue blocks from gastrectomy specimens for duodenal ulcer (2 cases) were stained with modified Giemsa and immunoenzymatic alkaline phosphatase - anti-alkaline phosphatase (APAAP) method, and were carefully examined for the presence of H. pylori. Results. Using a modified Giemsa stain, the spiral shaped bacteria of H. pylori stained blue, were attached to the brush border of the gastric foveolar epithelial cells. However, the specificity of modified Giemsa stain depended on the morphological appearance of H. pylori. The specificity of immunostaining permitted detection of low numbers or even single organisms. In all cases bacteria were more prominent and easier to detect in immunostained preparations. H. pylori was identified in 22 (73.3%) of 30 sections stained with modified Giemsa stain, but it could be identified with greater frequency in sections stained with APAAP, in 27 (90%) of 30 sections. Conclusion. Immunohistochemical identification of H. pylori was better than Giemsa stain for detecting that organism.

scholarly journals Helicobacter Pylori Eradication Therapy in both Erosive and Non-erosive Gastritis — A Prospective Study

2014 ◽  
Vol 4 (1) ◽  
pp. 15-20
Author(s):  
Mohammad Quamrul Hasan ◽  
MM Shahin-ul-Islam ◽  
Shahidul Hasan Mollick ◽  
Irin Perveen ◽  
ASMA Raihan
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Prospective Study ◽  
Rapid Urease Test ◽  
Erosive Gastritis ◽  
Endoscopic Findings ◽  
Urease Test ◽  
H Pylori ◽  
Gastric Malignancy ◽  
Better Than

Background: Infection with Helicobacter pylori (H. pylori) is a recognized cause of peptic ulcer and gastritis. Persistence of infection is a definite risk factor for gastric malignancy. Healing of gastritis after eradication of H. pylori reduces the risks of peptic ulcer disease and gastric malignancy. Objectives: To find out the relationship of H. pylori with erosive and nonerosive gastritis, the effect of anti-H. pylori therapy and to compare the effects of anti-H. pylori therapy between two types of gastritis. Materials and Methods: This prospective study was done in the Gastroenterology department of Bangabandhu Sheikh Mujib Medical University, Dhaka from June 2008 to May 2009. One hundred eighty dyspeptic patients were enrolled for the study. Patients with gastritis diagnosed by endoscopy underwent rapid urease test (RUT). RUT positive patients were considered to have H. pylori infection and were treated with triple therapy (omeprazole, amoxycillin and metronidiazole) for 14 days. Treatment responses were assessed by clinical history and also by endoscopic biopsy and RUT. Results of endoscopic findings and RUT after treatment were compared with pretreatment status. Results: Seventy patients completed the treatment and finally could be assessed. Endoscopic findings of 70 patients revealed that 56 (80%) patients had erosive gastritis and 14 (20%) patients had nonerosive gastritis. After treatment, 47 (67.1%) lesions became normal, 16 (22.9%) remained erosive and 7 (10%) non-erosive as before. Out of 14 non-erosive diseases, 7 became normal, while out of 56 erosive diseases 40 became normal. The erosive group responded significantly better than the non-erosive group (c2=32.766, p<0.001). Fifty nine (84.3%) patients with gastritis showed negative urease test after treatment. Conclusion: Strong relation between H. pylori infection and gastritis was found. Majority were antral erosive gastritis. Erosive group responded better than non-erosive group. DOI: http://dx.doi.org/10.3329/jemc.v4i1.18063 J Enam Med Col 2014; 4(1): 15-20

scholarly journals ChePep Controls Helicobacter pylori Infection of the Gastric Glands and Chemotaxis in the Epsilonproteobacteria

mBio ◽  
2011 ◽  
Vol 2 (4) ◽  
Author(s):  
Michael R. Howitt ◽  
Josephine Y. Lee ◽  
Paphavee Lertsethtakarn ◽  
Roger Vogelmann ◽  
Lydia-Marie Joubert ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Campylobacter Jejuni ◽  
Deep Sea ◽  
Hydrothermal Vent ◽  
Bacterial Chemotaxis ◽  
Peptic Ulcers ◽  
Gastric Glands ◽  
Content Type ◽  
H Pylori ◽  
Chemotaxis System

ABSTRACTMicrobes use directed motility to colonize harsh and dynamic environments. We discovered thatHelicobacter pyloristrains establish bacterial colonies deep in the gastric glands and identified a novel protein, ChePep, necessary to colonize this niche. ChePep is preferentially localized to the flagellar pole. Although mutants lacking ChePep have normal flagellar ultrastructure and are motile, they have a slight defect in swarming ability. By tracking the movement of single bacteria, we found that ∆ChePep mutants cannot control the rotation of their flagella and swim with abnormally frequent reversals. These mutants even sustain bursts of movement backwards with the flagella pulling the bacteria. Genetic analysis of the chemotaxis signaling pathway shows that ChePep regulates flagellar rotation through the chemotaxis system. By examiningH. pyloriwithin a microscopic pH gradient, we determined that ChePep is critical for regulating chemotactic behavior. ThechePepgene is unique to theEpsilonproteobacteriabut is found throughout this diverse group. We expressed ChePep from other members of theEpsilonproteobacteria, including the zoonotic pathogenCampylobacter jejuniand the deep sea hydrothermal vent inhabitantCaminibacter mediatlanticus, inH. pyloriand found that ChePep is functionally conserved across this class. ChePep represents a new family of chemotaxis regulators unique to theEpsilonproteobacteriaand illustrates the different strategies that microbes have evolved to control motility.IMPORTANCEHelicobacter pyloristrains infect half of all humans worldwide and contribute to the development of peptic ulcers and gastric cancer.H. pyloricannot survive within the acidic lumen of the stomach and uses flagella to actively swim to and colonize the protective mucus and epithelium. The chemotaxis system allowsH. pylorito navigate by regulating the rotation of its flagella. We identified a new protein, ChePep, which controls chemotaxis inH. pylori. ChePep mutants fail to colonize the gastric glands of mice and are completely outcompeted by normalH. pylori. Genes encoding ChePep are found only in the classEpsilonproteobacteria, which includes the human pathogenCampylobacter jejuniand environmental microbes like the deep-sea hydrothermal vent colonizerCaminibacter mediatlanticus, and we show that ChePep function is conserved in this class. Our study identifies a new colonization factor inH. pyloriand also provides insight into the control and evolution of bacterial chemotaxis.

scholarly journals Campylobacter jejuni Cytolethal Distending Toxin C Exploits Lipid Rafts to Mitigate Helicobacter pylori-Induced Pathogenesis

2021 ◽  
Vol 8 ◽  
Author(s):  
Jia-Yin Yeh ◽  
Hwai-Jeng Lin ◽  
Chia-Jung Kuo ◽  
Chun-Lung Feng ◽  
Chia-Huei Chou ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lipid Rafts ◽  
Campylobacter Jejuni ◽  
Nuclear Factor Kappa B ◽  
Gastrointestinal Diseases ◽  
Membrane Lipid ◽  
Cytolethal Distending Toxin ◽  
Vacuolating Cytotoxin ◽  
Cytotoxin Associated Gene A ◽  
H Pylori

Helicobacter pylori infection is associated with several gastrointestinal diseases, including gastritis, peptic ulcer, and gastrointestinal adenocarcinoma. Two major cytotoxins, vacuolating cytotoxin A (VacA) and cytotoxin-associated gene A (CagA), interact closely with lipid rafts, contributing to H. pylori-associated disease progression. The Campylobacter jejuni cytolethal distending toxin consists of three subunits: CdtA, CdtB, and CdtC. Among them, CdtA and CdtC bind to membrane lipid rafts, which is crucial for CdtB entry into cells. In this study, we employed recombinant CdtC (rCdtC) to antagonize the functions of H. pylori cytotoxin in cells. Our results showed that rCdtC alleviates cell vacuolation induced by H. pylori VacA. Furthermore, rCdtC reduces H. pylori CagA translocation, which decreases nuclear factor kappa-B activation and interleukin-8 production, resulting in the mitigation of gastric epithelial cell inflammation. These results reveal that CdtC hijacks cholesterol to compete for H. pylori cytotoxin actions via lipid rafts, ameliorating H. pylori-induced pathogenesis.

scholarly journals Heterologous production in Wolinella succinogenes and characterization of the quinol:fumarate reductase enzymes from Helicobacter pylori and Campylobacter jejuni

2006 ◽  
Vol 395 (1) ◽  
pp. 191-201 ◽  
Author(s):  
Mauro Mileni ◽  
Fraser MacMillan ◽  
Christos Tziatzios ◽  
Klaus Zwicker ◽  
Alexander H. Haas ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Membrane Protein ◽  
Campylobacter Jejuni ◽  
Pathogenic Bacteria ◽  
Analytical Ultracentrifugation ◽  
Detailed Comparison ◽  
Wolinella Succinogenes ◽  
Human Pathogens ◽  
H Pylori

The ϵ-proteobacteria Helicobacter pylori and Campylobacter jejuni are both human pathogens. They colonize mucosal surfaces causing severe diseases. The membrane protein complex QFR (quinol:fumarate reductase) from H. pylori has previously been established as a potential drug target, and the same is likely for the QFR from C. jejuni. In the present paper, we describe the cloning of the QFR operons from the two pathogenic bacteria H. pylori and C. jejuni and their expression in Wolinella succinogenes, a non-pathogenic ϵ-proteobacterium. To our knowledge, this is the first documentation of heterologous membrane protein production in W. succinogenes. We demonstrate that the replacement of the homologous enzyme from W. succinogenes with the heterologous enzymes yields mutants where fumarate respiration is fully functional. We have isolated and characterized the heterologous QFR enzymes. The high quality of the enzyme preparation enabled us to determine unequivocally by analytical ultracentrifugation the homodimeric state of the three detergent-solubilized heterotrimeric QFR enzymes, to accurately determine the different oxidation–reduction (‘redox’) midpoint potentials of the six prosthetic groups, the Michaelis constants for the quinol substrate, maximal enzymatic activities and the characterization of three different anti-helminths previously suggested to be inhibitors of the QFR enzymes from H. pylori and C. jejuni. This characterization allows, for the first time, a detailed comparison of the QFR enzymes from C. jejuni and H. pylori with that of W. succinogenes.

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