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Genome sequences of 65 Helicobacter pylori strains isolated from asymptomatic individuals and patients with gastric cancer, peptic ulcer disease, or gastritis.
Blanchard TG, Czinn SJ, Correa P, Nakazawa T, Keelan M, Morningstar L, Santana-Cruz I, Maroo A, McCracken C, Shefchek K, Daugherty S, Song Y, Fraser CM, Fricke WF
(2013) Pathog Dis 68: 39-43
MeSH Terms: Adult, Asymptomatic Diseases, Cluster Analysis, Colombia, DNA, Bacterial, Gastritis, Genome, Bacterial, Helicobacter Infections, Helicobacter pylori, Humans, Japan, Molecular Sequence Data, North America, Peptic Ulcer, Phylogeny, Sequence Analysis, DNA, Stomach Neoplasms
Show Abstract · Added September 3, 2013
Helicobacter pylori, inhabitant of the gastric mucosa of over half of the world population, with decreasing prevalence in the U.S., has been associated with a variety of gastric pathologies. However, the majority of H. pylori-infected individuals remain asymptomatic, and negative correlations between H. pylori and allergic diseases have been reported. Comprehensive genome characterization of H. pylori populations from different human host backgrounds including healthy individuals provides the exciting potential to generate new insights into the open question whether human health outcome is associated with specific H. pylori genotypes or dependent on other environmental factors. We report the genome sequences of 65 H. pylori isolates from individuals with gastric cancer, preneoplastic lesions, peptic ulcer disease, gastritis, and from asymptomatic adults. Isolates were collected from multiple locations in North America (USA and Canada) as well as from Columbia and Japan. The availability of these H. pylori genome sequences from individuals with distinct clinical presentations provides the research community with a resource for detailed investigations into genetic elements that correlate either positively or negatively with the epidemiology, human host adaptation, and gastric pathogenesis and will aid in the characterization of strains that may favor the development of specific pathology, including gastric cancer.
© 2013 Federation of European Microbiological Societies. Published by John Wiley & Sons Ltd. All rights reserved.
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17 MeSH Terms
Helicobacter pylori VacA induces programmed necrosis in gastric epithelial cells.
Radin JN, González-Rivera C, Ivie SE, McClain MS, Cover TL
(2011) Infect Immun 79: 2535-43
MeSH Terms: Adenosine Triphosphate, Bacterial Proteins, Bacterial Toxins, Blotting, Western, Caspases, Cell Death, Cell Line, Cell Line, Tumor, Epithelial Cells, Gastric Mucosa, Gastritis, HMGB1 Protein, Helicobacter pylori, Humans, Ion Channels, L-Lactate Dehydrogenase, Necrosis, Peptic Ulcer, Poly(ADP-ribose) Polymerases, Stomach Neoplasms, Virulence Factors
Show Abstract · Added March 5, 2014
Helicobacter pylori is a Gram-negative bacterium that colonizes the human stomach and contributes to the development of peptic ulcer disease and gastric cancer. The secreted pore-forming toxin VacA is one of the major virulence factors of H. pylori. In the current study, we show that AZ-521 human gastric epithelial cells are highly susceptible to VacA-induced cell death. Wild-type VacA causes death of these cells, whereas mutant VacA proteins defective in membrane channel formation do not. Incubation of AZ-521 cells with wild-type VacA results in cell swelling, poly(ADP-ribose) polymerase (PARP) activation, decreased intracellular ATP concentration, and lactate dehydrogenase (LDH) release. VacA-induced death of these cells is a caspase-independent process that results in cellular release of histone-binding protein high mobility group box 1 (HMGB1), a proinflammatory protein. These features are consistent with the occurrence of cell death through a programmed necrosis pathway and suggest that VacA can be included among the growing number of bacterial pore-forming toxins that induce cell death through programmed necrosis. We propose that VacA augments H. pylori-induced mucosal inflammation in the human stomach by causing programmed necrosis of gastric epithelial cells and subsequent release of proinflammatory proteins and may thereby contribute to the pathogenesis of gastric cancer and peptic ulceration.
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21 MeSH Terms
Risk of peptic ulcer hospitalizations in users of NSAIDs with gastroprotective cotherapy versus coxibs.
Ray WA, Chung CP, Stein CM, Smalley WE, Hall K, Arbogast PG, Griffin MR
(2007) Gastroenterology 133: 790-8
MeSH Terms: Adult, Aged, Anti-Inflammatory Agents, Non-Steroidal, Anti-Ulcer Agents, Arthritis, Rheumatoid, Cohort Studies, Cyclooxygenase 2 Inhibitors, Dose-Response Relationship, Drug, Drug Therapy, Combination, Female, Gastrointestinal Tract, Histamine H2 Antagonists, Hospitalization, Humans, Incidence, Male, Middle Aged, Osteoarthritis, Peptic Ulcer, Proton Pump Inhibitors, Risk Factors
Show Abstract · Added December 10, 2013
BACKGROUND & AIMS - The primary strategies to reduce the risk of serious gastropathy caused by traditional nonsteroidal anti-inflammatory drugs (NSAIDs) are use of a coxib or concurrent use of a proton pump inhibitor or double-dose histamine-2 receptor antagonist. However, the relative clinical effectiveness of these therapeutic alternatives is understudied.
METHODS - We studied peptic ulcer hospitalizations in a cohort of Tennessee Medicaid enrollees between 1996 and 2004. To decrease potential "channeling" bias, the study included only new episodes of prescribed NSAID or coxib use and controlled for multiple baseline risk factors for upper gastrointestinal disease. There were 234,010 and 48,710 new episodes of NSAID and coxib use, respectively, with 363,037 person-years of follow-up and 1223 peptic ulcer hospitalizations.
RESULTS - Current users of NSAIDs with no gastroprotective cotherapy had an adjusted incidence of peptic ulcer hospitalizations of 5.65 per 1000 person-years, 2.76 (95% confidence interval, 2.35-3.23) times greater than that for persons not currently using either NSAIDs or coxibs. This risk was reduced by 39% (16%-56%, 95% CI) for current users of NSAIDs with gastroprotective cotherapy and 40% (23%-54%) for current users of coxibs without such cotherapy. Concurrent users of NSAIDs and proton pump inhibitors had a 54% (27%-72%) risk reduction, very similar to the 50% (27%-66%) reduction for concurrent users of proton pump inhibitors and coxibs.
CONCLUSIONS - These findings suggest that coprescribing a proton pump inhibitor with an NSAID is as effective as use of a coxib for reducing the risk of NSAID-induced gastropathy.
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21 MeSH Terms
Gastrointestinal complications associated with hepatic arterial Yttrium-90 microsphere therapy.
Murthy R, Brown DB, Salem R, Meranze SG, Coldwell DM, Krishnan S, Nunez R, Habbu A, Liu D, Ross W, Cohen AM, Censullo M
(2007) J Vasc Interv Radiol 18: 553-61; quiz 562
MeSH Terms: Adenocarcinoma, Adult, Aged, Brachytherapy, Embolization, Therapeutic, Gastrointestinal Tract, Hepatic Artery, Humans, Injections, Intra-Arterial, Liver Neoplasms, Male, Microspheres, Peptic Ulcer, Peptic Ulcer Hemorrhage, Radionuclide Imaging, Radiopharmaceuticals, Retrospective Studies, Technetium Tc 99m Aggregated Albumin, Yttrium Radioisotopes
Show Abstract · Added March 5, 2014
Hepatic arterial therapy with yttrium-90 microspheres exploits the avenue provided by the neoplastic microvasculature to deliver high-energy, low-penetrating therapeutic doses of radiation. Variant hepatic arterial anatomy, collateral vessels, and changes in flow dynamics during treatment can affect particle dispersion and lead to nontarget particle distribution and subsequent gastrointestinal morbidity. Awareness of these variances and techniques to prevent gastrointestinal tract microsphere delivery is essential in mitigating this serious complication. Our aim is to increase the understanding of the role of various imaging and preventative techniques in minimizing this undesired effect.
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19 MeSH Terms
The association of cigarette smoking with self-reported disease before middle age: the Coronary Artery Risk Development in Young Adults (CARDIA) study.
Hozawa A, Houston T, Steffes MW, Widome R, Williams OD, Iribarren C, Pletcher MJ, Daviglus ML, Carr JJ, Jacobs DR
(2006) Prev Med 42: 193-9
MeSH Terms: Adolescent, Adult, African Continental Ancestry Group, Cardiovascular Diseases, Chronic Disease, European Continental Ancestry Group, Female, Humans, Incidence, Male, Neoplasms, Peptic Ulcer, Proportional Hazards Models, Respiratory Tract Diseases, Risk Assessment, Risk Factors, Smoking, Smoking Cessation, Time Factors, Tobacco Smoke Pollution, United States
Show Abstract · Added February 15, 2014
BACKGROUND - Evidence that demonstrates the harmful effect of cigarette smoking during young adulthood is limited. Therefore, we assessed associations between cigarette smoking and several self-reported illnesses in a prospective cohort study in healthy young adults.
METHODS - Data were derived from 4472 adults aged 18 to 30 years at baseline participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study and reexamined at least once after 7, 10, or 15 years.
RESULTS - Cigarette smoking in 1985-86 was related to self-reported smoking-related cancers, circulatory disease, and peptic ulcer. Incidence of these diseases was 9.3/1000 person years among current smokers vs. 4.5/1000 person years among never smokers with no exposure to passive smoke, relative risk (adjusted for race, sex, education, and center) 1.96 (1.42-2.70). Assuming causal relationships, 32% of these premature incidents were attributable to smoking. The relative risks of liver disease, migraine headache, depression, being ill the day before the examination, and chronic cough and phlegm production were also higher in smokers.
CONCLUSIONS - Smokers aged 18-30 followed for 7 to 15 years reported an excess of both major and minor ailments related to earlier and current smoking. Thus, prevention, cessation, and avoiding passive smoking should remain strong goals among young people.
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21 MeSH Terms
Helicobacter pylori VacA, a paradigm for toxin multifunctionality.
Cover TL, Blanke SR
(2005) Nat Rev Microbiol 3: 320-32
MeSH Terms: Animals, Antigen Presentation, Bacterial Proteins, Bacterial Toxins, Epithelial Cells, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Peptic Ulcer, Phagocytosis, Stomach Neoplasms, T-Lymphocytes, Virulence
Show Abstract · Added March 5, 2014
Bacterial protein toxins alter eukaryotic cellular processes and enable bacteria to successfully colonize their hosts. In recent years, there has been increased recognition that many bacterial toxins are multifunctional proteins that can have pleiotropic effects on mammalian cells and tissues. In this review, we examine a multifunctional toxin (VacA) that is produced by the bacterium Helicobacter pylori. The actions of H. pylori VacA represent a paradigm for how bacterial secreted toxins contribute to colonization and virulence in multiple ways.
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14 MeSH Terms
Underutilization of gastroprotective measures in patients receiving nonsteroidal antiinflammatory drugs.
Smalley W, Stein CM, Arbogast PG, Eisen G, Ray WA, Griffin M
(2002) Arthritis Rheum 46: 2195-200
MeSH Terms: Anti-Inflammatory Agents, Non-Steroidal, Anti-Ulcer Agents, Comorbidity, Cross-Sectional Studies, Cyclooxygenase Inhibitors, Digestive System, Drug Therapy, Combination, Female, Humans, Male, Peptic Ulcer, Risk Factors, Tennessee
Show Abstract · Added December 10, 2013
OBJECTIVE - To determine the frequency of use of recommended gastroprotective strategies in a cohort of patients receiving recurrent treatment with nonsteroidal antiinflammatory drugs (NSAIDs).
METHODS - A cross-sectional study was performed using administrative data from the Tennessee Medicaid (TennCare) program. The study population consisted of 76,765 recurrent recipients of NSAIDs (NSAID users), comprising 24% of the 319,402 persons ages 50 years or older enrolled in the TennCare program from January 1999 through June 2000. Frequency of use of either of 2 recommended gastroprotective strategies, involving either traditional NSAIDs combined with recommended anti-ulcer cotherapy or use of a selective cyclooxygenase 2-inhibiting drug (coxib), was measured and categorized by risk for ulcer complication.
RESULTS - Among this cohort of recurrent NSAID users, 16% received 1 of the 2 recommended gastroprotective therapies: 10% received traditional NSAIDs along with antiulcer drugs at the recommended doses and 6% received coxibs. Among those patients with > or=2 risk factors for ulcer complications (age 75 years or older, peptic ulcer or gastrointestinal bleeding in the past year, or concurrent use of oral anticoagulants or corticosteroids), 30% received such gastroprotective therapy.
CONCLUSION - Use of recommended strategies to decrease ulcer complications in vulnerable populations is relatively uncommon.
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13 MeSH Terms
Is there a place for non-selective NSAIDs in the treatment of arthritis?
Crofford LJ
(2002) Joint Bone Spine 69: 4-7
MeSH Terms: Animals, Anti-Inflammatory Agents, Non-Steroidal, Arthritis, Cyclooxygenase 1, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, Humans, In Vitro Techniques, Isoenzymes, Membrane Proteins, Peptic Ulcer, Prostaglandin-Endoperoxide Synthases
Added September 18, 2013
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13 MeSH Terms
Analysis of iceA genotypes in South African Helicobacter pylori strains and relationship to clinically significant disease.
Kidd M, Peek RM, Lastovica AJ, Israel DA, Kummer AF, Louw JA
(2001) Gut 49: 629-35
MeSH Terms: Adenocarcinoma, Animals, Bacterial Outer Membrane Proteins, Bacterial Proteins, Blotting, Southern, Gastritis, Genes, Bacterial, Genetic Heterogeneity, Helicobacter Infections, Helicobacter pylori, Humans, Peptic Ulcer, Polymerase Chain Reaction, Protein Structure, Secondary, Sequence Analysis, DNA, Stomach Neoplasms, Virulence
Show Abstract · Added October 15, 2015
BACKGROUND - South African Helicobacter pylori isolates are characterised by the universal presence of cagA but have differences in vacuolating cytotoxin gene (vacA) alleles which correlate with clinically significant disease. However, the candidate virulence marker gene iceA has not been investigated.
AIM - To characterise the genetic organisation and heterogeneity of iceA genotypes in different South African clinical isolates.
PATIENTS AND METHODS - We studied H pylori strains isolated from 86 dyspeptic patients (30 with peptic ulcer disease (PUD), 19 with distal gastric adenocarcinoma (GC), and 37 with non-erosive gastritis) for the presence of iceA1 or iceA2 genes, and for differences in the genetic organisation of iceA2 by polymerase chain reaction, Southern hybridisation analysis, and sequencing.
RESULTS - Genetic analysis of iceA1 demonstrated significant homology (92-95%) with the USA type strain 26695 and probably functions as a transcriptional regulator, while a novel variant (iceA2D') of iceA2 and marked differences in predicted protein secondary structure of the iceA2 protein were defined. iceA1 was detected in 68% and iceA2 in 80% of all clinical isolates. Although approximately 40% of patients had both strains, a higher prevalence (p< 0.01) of GC patients were infected with iceA1 isolates which were invariably vacA s1/iceA1 (p< 0.005 v gastritis). Isolates from PUD patients were distinguished by the structurally altered iceA2D variant (53%; p<0.03 v gastritis) while the iceA2C variant distinguished isolates from patients with gastritis alone (67%; p< 0.005 v PUD).
CONCLUSION - In this study, an association between iceA1 and GC was noted while differences in variants of iceA2 differentiated between PUD and gastritis alone. Combination analyses of iceA genotypes and vacA alleles supported these associations.
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17 MeSH Terms
The biological impact of Helicobacter pylori colonization.
Peek RM
(2001) Semin Gastrointest Dis 12: 151-66
MeSH Terms: Antigens, Bacterial, Bacterial Proteins, Biopsy, Breath Tests, Gastritis, Helicobacter Infections, Helicobacter pylori, Humans, Peptic Ulcer, Polymerase Chain Reaction, Serologic Tests, Stomach Neoplasms, Urea, Urease
Show Abstract · Added March 5, 2014
Helicobacterpylori causes persistent inflammation in the human stomach, yet only a minority of persons harboring this organism develop peptic ulcer disease or gastric malignancy. H. pylori isolates possess substantial phenotypic and genotypic diversity, which may engender differential host inflammatory responses that influence clinical outcome. For example, strains that possess the cag pathogenicity island induce more severe gastritis and augment the risk for developing peptic ulcer disease and distal gastric cancer. However, important geographic differences in susceptibility to disease exist as clear-cut markers for H. pylori strains that affect certain groups of colonized individuals have little or no predictive power for other populations. Recent investigations that have more precisely delineated mechanisms of H. pylori pathogenesis will ultimately help to define which colonized persons bear the highest risk for subsequent development of clinical disease, and thus enable physicians to appropriately focus diagnostic testing and eradication therapy. Although stratification of disease risk based on H. pylori strain characteristics is unlikely to completely account for differences in clinical outcomes, it is an important first step in helping to understand the biology of long-term interactions between H. pylori and its human host.
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14 MeSH Terms