scholarly journals Helicobacter pylori genotyping from positive clotests in patients with duodenal ulcer

2000 ◽  
Vol 55 (5) ◽  
pp. 155-160 ◽  
Author(s):  
Rejane Mattar ◽  
Antonio Atílio Laudanna
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Virulent Strain ◽  
Normal Population ◽  
Human Stomach ◽  
Caga Status ◽  
H Pylori ◽  
Multiple Strains

Even though the seroprevalence of H. pylori may be high in the normal population, a minority develops peptic ulcer. Colonization of the gastric mucosa by more pathogenic vacA strains of H. pylori seems to be associated with enhanced gastric inflammation and duodenal ulcer. H. pylori genotyping from positive CLOtests was developed to determine the vacA genotypes and cagA status in 40 duodenal ulcer patients and for routine use. The pathogenic s1b/ m1/ cagA genotype was the most frequently occurring strain (17/42.5%); only two (5%) patients presented the s2/ m2 genotype, the less virulent strain. Multiple strains were also detected in 17 (42.5%) patients. Multiple strains of H. pylori colonizing the human stomach have been underestimated, because genotyping has been performed from cultures of H. pylori. We concluded that genotyping of H. pylori from a positive CLOtest had the advantages of reducing the number of biopsies taken during endoscopy, eliminating the step of culturing H. pylori, and assuring the presence of H. pylori in the specimen being processed.

scholarly journals Helicobacter pyloriAnti-CagA Antibodies: Prevalence in Symptomatic and Asymptomatic Subjects in Turkey

2002 ◽  
Vol 16 (8) ◽  
pp. 527-532 ◽  
Author(s):  
M Fatih Abasiyanik ◽  
Ersan Sander ◽  
Barik A Salih
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Chronic Gastritis ◽  
Molecular Weights ◽  
Cancer Antigens ◽  
Gastroduodenal Disease ◽  
H Pylori ◽  
Asymptomatic Subjects

BACKGROUND: Several reports have shown the prevalence of anti-CagA antibodies to be associated with the development of peptic ulcer diseases, while others have indicated that there is no such association.AIM: To examine the prevalence of antibodies to CagA and otherHelicobacter pyloriantigens in symptomatic and asymptomatic subjects in Turkey.SUBJECTS AND METHODS: Sixty-six symptomatic subjects, 16 to 74 years of age, were examined forH pyloriby biopsy-based tests and ELISA. One hundred nineteen asymptomatic subjects, 20 to 65 years of age, were also tested serologically for the presence ofH pylori. Samples from both groups that were found to be positive forH pyloriby ELISA were then tested by immunoblotting.RESULTS: Fifty-four (82%) symptomatic subjects and 76 (64%) asymptomatic subjects were found to beH pylori-positive by ELISA. Samples from 30 symptomatic subjects who were found to beH pylori-positive by ELISA were analyzed by immunoblotting. Antibodies to CagA (116 kDa) antigen were detected in immunoblots of 11 of 14 (79%) with chronic gastritis, 12 of 13 (92%) with duodenal ulcer and three of three (100%) with gastric cancer. Antigens of the following molecular weights were also detected in these 30 subjects: 89 kDa (VacA) in 21 (70%), 37 kDa in 21 (70%), 35 kDa in 19 (63%), 30 kDa in 27 (90%) and 19.5 kDa in 19 (63%). Immunoblots of 40 ELISA-positive asymptomatic subjects showed that 33 (83%) had antibodies to CagA antigen, 26 (65%) to VacA antigen, 30 (75%) to a 37 kDa antigen, 30 (75%) to a 35 kDa antigen, 39 (98%) to a 30 kDa antigen and 36 (90%) to a 19.5 kDa antigen.CONCLUSIONS: Antibodies to CagA antigen were prevalent in both groups, regardless of the presence of gastroduodenal disease.

scholarly journals Prevalence of Helicobacter pylori infection among patients undergoing upper gastrointestinal endoscopy

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Vudumula Vijaya Lakshmi
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Normal Population ◽  
Gastric Ulcers ◽  
Upper Gastrointestinal Endoscopy ◽  
Contributing Factors ◽  
Duodenal Ulcers ◽  
Female Ratio ◽  
Ulcer Disease ◽  
H Pylori

Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. This study was under taken at the Department of surgery, Narayana medical college, Nellore from January 2007 to July 2008. A total of 150 patients with duodenal ulcers, gastric ulcers, antral gastritis, gastric carcinoma and dyspepsia of any kind were studied. Maximum number of cases were in the age group of 31 years to 50 years among both sexes and number of cases gradually decreased after 50 years of age in males and females. Males were more in number and male to female ratio is (2.75:1) approximately 3:1.

scholarly journals Helicobacter pylori–binding nonacid glycosphingolipids in the human stomach

2018 ◽  
Vol 293 (44) ◽  
pp. 17248-17266 ◽  
Author(s):  
Chunsheng Jin ◽  
Angela Barone ◽  
Thomas Borén ◽  
Susann Teneberg
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Structural Complexity ◽  
Human Stomach ◽  
Carbohydrate Binding ◽  
Human Gastric Mucosa ◽  
H Pylori ◽  
Contrast Information

Helicobacter pylori has a number of well-characterized carbohydrate-binding adhesins (BabA, SabA, and LabA) that promote adhesion to the gastric mucosa. In contrast, information on the glycoconjugates present in the human stomach remains unavailable. Here, we used MS and binding of carbohydrate-recognizing ligands to characterize the glycosphingolipids of three human stomachs from individuals with different blood group phenotypes (O(Rh−)P, A(Rh+)P, and A(Rh+)p), focusing on compounds recognized by H. pylori. We observed a high degree of structural complexity, and the composition of glycosphingolipids differed among individuals with different blood groups. The type 2 chain was the dominating core chain of the complex glycosphingolipids in the human stomach, in contrast to the complex glycosphingolipids in the human small intestine, which have mainly a type 1 core. H. pylori did not bind to the O(Rh−)P stomach glycosphingolipids, whose major complex glycosphingolipids were neolactotetraosylceramide, the Lex, Lea, and H type 2 pentaosylceramides, and the Ley hexaosylceramide. Several H. pylori-binding compounds were present among the A(Rh+)P and A(Rh+)p stomach glycosphingolipids. Ligands for BabA-mediated binding of H. pylori were the Leb hexaosylceramide, the H type 1 pentaosylceramide, and the A type 1/ALeb heptaosylceramide. Additional H. pylori-binding glycosphingolipids recognized by BabA-deficient strains were lactosylceramide, lactotetraosylceramide, the x2 pentaosylceramide, and neolactohexaosylceramide. Our characterization of human gastric receptors required for H. pylori adhesion provides a basis for the development of specific compounds that inhibit the binding of this bacterium to the human gastric mucosa.

scholarly journals Gene structure of the Helicobacter pylori cytotoxin and evidence of its key role in gastric disease.

1994 ◽  
Vol 179 (5) ◽  
pp. 1653-1658 ◽  
Author(s):  
J L Telford ◽  
P Ghiara ◽  
M Dell'Orco ◽  
M Comanducci ◽  
D Burroni ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Chronic Infection ◽  
Gastric Disease ◽  
Human Gastric Mucosa ◽  
Gastric Lesions ◽  
Gram Negative ◽  
H Pylori ◽  
Cytotoxin Gene

The gram negative, microaerophilic bacterium Helicobacter pylori colonizes the human gastric mucosa and establishes a chronic infection that is tightly associated with atrophic gastritis, peptic ulcer, and gastric carcinoma. Cloning of the H. pylori cytotoxin gene shows that the protein is synthesized as a 140-kD precursor that is processed to a 94-kD fully active toxin. Oral administration to mice of the purified 94-kD protein caused ulceration and gastric lesions that bear some similarities to the pathology observed in humans. The cloning of the cytotoxin gene and the development of a mouse model of human gastric disease will provide the basis for the understanding of H. pylori pathogenesis and the development of therapeutics and vaccines.

scholarly journals Review of Research on Routes of Helicobacter pylori Infection

2015 ◽  
Vol 4 (2) ◽  
pp. 45-49
Author(s):  
Hang Li
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Gastric Adenocarcinoma ◽  
Precancerous Lesions ◽  
Natural Environments ◽  
H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

scholarly journals Helicobacter pylori: Basic Mechanisms to Clinical Cure

1995 ◽  
Vol 9 (2) ◽  
pp. 91-95 ◽  
Author(s):  
ABR Thomson ◽  
CN Williams
Keyword(s):  
Gastric Cancer ◽  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Clinical Cure ◽  
Eradication Therapy ◽  
Dual Therapy ◽  
Quadruple Therapy ◽  
Ulcer Disease ◽  
H Pylori

Since its rediscovery 10 years ago,Helicobacter pylorihas reshaped our thinking about the course of peptic ulcer disease. Our approach to the patient with a duodenal ulcer has become one of attempting eradication therapy at the time of first diagnosis, in the hope of curing the ulcer disease. Gastric and duodenal ulceration are only two of the manifestations of this chronic antral infection; other complications ofH pyloriinclude gastritis, gastric cancer and possible maltomas. Therapy ofH pyloriinfection is complicated and involves dual therapy with an antibiotic plus a protein pump inhibitor, such as omeprazole 20 mg bid plus amoxicillin 1 g bid for two weeks, triple or quadruple therapy with bismuth, two antibiotics and an H2-receptor antagonist. Vaccination againstH pyloriis on the far horizon.

scholarly journals Prevalence of AntiHelicobacter pylori Antibodies among Students of Cihan University, Erbil

2019 ◽  
Vol 3 (1) ◽  
pp. 66-70
Author(s):  
Sarah Hoshyar Maroof ◽  
Hadi Mahdi Alsakee ◽  
Gulistan Hussein Muhammad ◽  
Asia Sherzad Muhammad ◽  
Ilaf Abdulrazaq Rashid ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Abdominal Pain ◽  
Chronic Disease ◽  
University Students ◽  
Epigastric Pain ◽  
Tap Water ◽  
Human Stomach ◽  
Blood Samples ◽  
H Pylori

Helicobacter pylori is resident in human stomach and causes chronic disease (peptic ulcer and gastritis). The mouth and colon were both known to host a large number of microbes. This study was carried out to investigate the seroprevalence of H. pylori infection among Cihan University students. A total of 197 blood samples were collected from the students (53 females and 144 males) from 13 departments of Cihan University, Erbil, and tested for anti-H. pylori antibodies, using rapid immunochromatography assay. Among 197 students tested, 44 (22.3%) showed positive reaction for H. pylori, 32 males and 12 females. It was non-significantly higher among students with ages ranged between 29 and 32 years old. Twenty-one of infected students were using tap water for drinking. Twenty-six (59.1%) of positive students experienced no symptoms and 18 (40.9%) were symptomatic (13.63% epigastric pain and 27.2% abdominal pain).

scholarly journals Gastric Helicobacters in Domestic Animals and Nonhuman Primates and Their Significance for Human Health

2009 ◽  
Vol 22 (2) ◽  
pp. 202-223 ◽  
Author(s):  
Freddy Haesebrouck ◽  
Frank Pasmans ◽  
Bram Flahou ◽  
Koen Chiers ◽  
Margo Baele ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Lymphoid Tissue ◽  
Direct Contact ◽  
Nonhuman Primates ◽  
Domestic Animals ◽  
Human Stomach ◽  
Gastric Ulcers ◽  
H Pylori

SUMMARY Helicobacters other than Helicobacter pylori have been associated with gastritis, gastric ulcers, and gastric mucosa-associated lymphoid tissue lymphoma in humans. These very fastidious microorganisms with a typical large spiral-shaped morphology were provisionally designated “H. heilmannii,” but in fact they comprise at least five different Helicobacter species, all of which are known to colonize the gastric mucosa of animals. H. suis, which has been isolated from the stomachs of pigs, is the most prevalent gastric non-H. pylori Helicobacter species in humans. Other gastric non-H. pylori helicobacters colonizing the human stomach are H. felis, H. salomonis, H. bizzozeronii, and the still-uncultivable “Candidatus Helicobacter heilmannii.” These microorganisms are often detected in the stomachs of dogs and cats. “Candidatus Helicobacter bovis” is highly prevalent in the abomasums of cattle but has only occasionally been detected in the stomachs of humans. There are clear indications that gastric non-H. pylori Helicobacter infections in humans originate from animals, and it is likely that transmission to humans occurs through direct contact. Little is known about the virulence factors of these microorganisms. The recent successes with in vitro isolation of non-H. pylori helicobacters from domestic animals open new perspectives for studying these microorganisms and their interactions with the host.

scholarly journals Polyphenols Reduce Gastritis Induced by Helicobacter pylori Infection or VacA Toxin Administration in Mice

2006 ◽  
Vol 50 (7) ◽  
pp. 2550-2552 ◽  
Author(s):  
P. Ruggiero ◽  
F. Tombola ◽  
G. Rossi ◽  
L. Pancotto ◽  
L. Lauretti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Gastric Epithelium ◽  
Human Gastric Mucosa ◽  
H Pylori

ABSTRACT Helicobacter pylori colonizes the human gastric mucosa, causing inflammation that leads to atrophic gastritis, and it can cause peptic ulcer and gastric cancer. We show that polyphenol administration to mice experimentally infected by H. pylori or treated with VacA toxin can limit gastric epithelium damage, an effect that may be linked to VacA inhibition.

Exopolysaccharide-producing Streptococcus thermophilus CRL1190 reduces the inflammatory response caused by Helicobacter pylori

2017 ◽  
Vol 8 (3) ◽  
pp. 451-461 ◽  
Author(s):  
G. Marcial ◽  
J. Villena ◽  
G. Faller ◽  
A. Hensel ◽  
G. Font de Valdéz
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Inflammatory Response ◽  
Streptococcus Thermophilus ◽  
Human Stomach ◽  
Epithelial Cell Line ◽  
Ags Cells ◽  
Tissue Samples ◽  
H Pylori

This work evaluated the ability of the probiotic Streptococcus thermophilus CRL1190 strain and its exopolysaccharides to adhere to gastric mucosa. Probiotic bacteria attachment to the human stomach epithelium was confirmed in human stomach tissue samples and the gastric epithelial cell line AGS. In addition, it was demonstrated that S. thermophilus CRL1190 strain reduced Helicobacter pylori adhesion and attenuated inflammatory response in AGS cells. This is the first demonstration of the capacity of S. thermophilus CRL1190 to adhere to the stomach gastric mucosa, and improve protection against H. pylori through the reduction of its adhesion and the modulation of the inflammatory response. Therefore, S. thermophilus CRL1190 fermented milk is a good candidate for further in vivo studying of the protective effect of functional food against H. pylori infection and gastric inflammatory damage.

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