oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Prevalence and clinical relevance of Helicobacter pylori cagA and vacA genes in Lebanese patients with gastritis and peptic ulcer disease
Aline E.Khayat,1 Assaad M. Soweid,2 Mireille M. Kattar,3 Ayman N. Tawil,3 Ihab I. El Hajj,2 Cecilio Azar,2 Benjamin D. Gold,4 and Ghassan M. Matar.1
Journal of Infection in Developing Countries , 2007,
Abstract: Background: The prevalence and clinical relevance of H. pylori cagA and vacA virulence genes in the pathogenesis of disease phenotype was assessed by a novel approach for this organism consisting of determination and comparisons of H. pylori gene transcription levels directly in gastric biopsies according to disease phenotype.Methodology: Gastric mucosal biopsies were collected from patients with peptic ulcer disease (PUD), gastritis, and normal mucosa in an academic medical center in Lebanon. H. pylori was detected in these biopsies by rapid urease (CLO ) test and PCR amplification of the ureA gene. H. pylori virulence genes, their transcription and transcription levels were determined respectively by PCR, RT-PCR and real time RT-PCR. Results: Forty-five percent of patients were H. pylori positive by PCR of the ureA gene, 37.5% of whom had cagA and 59.4% vacA.Conclusions: The cagA and vacA genes were detected more frequently in PUD patients with significantly higher transcription levels than in gastritis and normal mucosa.
Frequency of vacA, cagA and babA2 virulence markers in Helicobacter pylori strains isolated from Mexican patients with chronic gastritis
Gloria Paniagua, Eric Monroy, Raymundo Rodríguez, Salvador Arroniz, Cristina Rodríguez, José Cortés, Ausencio Camacho, Erasmo Negrete, Sergio Vaca
Annals of Clinical Microbiology and Antimicrobials , 2009, DOI: 10.1186/1476-0711-8-14
Abstract: H. pylori was identified in cultures of gastric biopsies by nested PCR. vacA and cagA genes were detected by multiplex PCR, whereas babA2 gene was identified by conventional PCR.H. pylori-positive biopsies were 143 (60.1%). All H. pylori strains were vacA+; 39.2% were cagA+; 13.3% were cagA+ babA2+ and 8.4% were babA2+. Mexican strains examined possessed the vacA s1, m1 (43.4%), s1, m2 (24.5%), s2, m1 (20.3%) and s2, m2 (11.9%) genotypes.These results show that the Mexican patients suffering chronic gastritis we have studied had a high incidence of infection by H. pylori. Forty four percent (63/143) of the H. pylori strains analyzed in this work may be considered as highly virulent since they possessed two or three of the virulence markers analyzed: vacA s1 cagA babA2 (9.8%, 14/143), vacA s1 babA2 (4.9%, 7/143), and vacA s1 cagA (29.4%, 42/143). However, a statistically significant correlation was not observed between vacAs1, cagA and babA2 virulence markers (χ2 test; P > 0.05).Helicobacter pylori is a spiral-shaped Gram-negative bacterium that has been strongly associated with chronic gastritis and peptic ulcer disease [1,2], and it is a risk factor for gastric cancer [3-5]Three major virulence factors of H. pylori have been described: the cytotoxin-associated gene product (CagA), the vacuolating toxin (VacA) and the adhesion protein BabA2. The cytotoxin-associated gene A (CagA) is a protein with a molecular mass of approximately 125–140 kDa, encoded by the cagA gene, [6,7], that is translocated into gastric epithelial cells by a type IV secretion system, encoded by the cag pathogenicity island (cag PAI) [8]. Inside epithelial cells CagA is phosphorylated on tyrosine residues by host cell Src kinases and stimulates cell-signaling pathways [9], which in turn causes elongation of the cell [10] and activation of proto-oncogenes [11].The vacuolating cytotoxin gene vacA is polymorphic, varying in the signal and middle regions. The main signal region alleles are s1 and s
Helicobacter pylori Counteracts the Apoptotic Action of Its VacA Toxin by Injecting the CagA Protein into Gastric Epithelial Cells  [PDF]
Amanda Oldani equal contributor,Mireille Cormont equal contributor,Veronique Hofman equal contributor,Valentina Chiozzi,Olivier Oregioni,Alexandra Canonici,Anna Sciullo,Patrizia Sommi,Alessia Fabbri,Vittorio Ricci ? ,Patrice Boquet ?
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000603
Abstract: Infection with Helicobacter pylori is responsible for gastritis and gastroduodenal ulcers but is also a high risk factor for the development of gastric adenocarcinoma and lymphoma. The most pathogenic H. pylori strains (i.e., the so-called type I strains) associate the CagA virulence protein with an active VacA cytotoxin but the rationale for this association is unknown. CagA, directly injected by the bacterium into colonized epithelium via a type IV secretion system, leads to cellular morphological, anti-apoptotic and proinflammatory effects responsible in the long-term (years or decades) for ulcer and cancer. VacA, via pinocytosis and intracellular trafficking, induces epithelial cell apoptosis and vacuolation. Using human gastric epithelial cells in culture transfected with cDNA encoding for either the wild-type 38 kDa C-terminal signaling domain of CagA or its non-tyrosine-phosphorylatable mutant form, we found that, depending on tyrosine-phosphorylation by host kinases, CagA inhibited VacA-induced apoptosis by two complementary mechanisms. Tyrosine-phosphorylated CagA prevented pinocytosed VacA to reach its target intracellular compartments. Unphosphorylated CagA triggered an anti-apoptotic activity blocking VacA-induced apoptosis at the mitochondrial level without affecting the intracellular trafficking of the toxin. Assaying the level of apoptosis of gastric epithelial cells infected with wild-type CagA+/VacA+ H. pylori or isogenic mutants lacking of either CagA or VacA, we confirmed the results obtained in cells transfected with the CagA C-ter constructions showing that CagA antagonizes VacA-induced apoptosis. VacA toxin plays a role during H. pylori stomach colonization. However, once bacteria have colonized the gastric niche, the apoptotic action of VacA might be detrimental for the survival of H. pylori adherent to the mucosa. CagA association with VacA is thus a novel, highly ingenious microbial strategy to locally protect its ecological niche against a bacterial virulence factor, with however detrimental consequences for the human host.
Helicobacter pylori cagA and vacA genotypes in Cuban and Venezuelan populations
Ortiz-Princz, Diana;Guariglia-Oropeza, Verónica;ávila, Maira;Correnti, María;Perrone, Marianella;Gutierrez, Beatriz;Torres, Javier;Megraud, Francis;Cavazza, María Eugenia;
Memórias do Instituto Oswaldo Cruz , 2010, DOI: 10.1590/S0074-02762010000300016
Abstract: the aim of this study was to determine the presence of helicobacter pylori cytotoxin-associated gene (caga)/vacuolating cytotoxin gene (vaca) among patients with chronic gastritis in cuba and venezuela. gastric antrum biopsies were taken for culture, dna extraction and pcr analysis. amplification of vaca and caga segments was performed using two regions of caga: 349 bp were amplified with the f1/b1 primers and the remaining 335 bp were amplified with the b7629/b7628 primers. the va1-f/va1-r set of primers was used to amplify the 259-bp (s1) or 286-bp (s2) product and the vag-r/vag-f set of primers was used to amplify the 567-bp (m1) or 642-bp (m2) regions of vaca. caga was detected in 87% of the antral samples from cuban patients and 80.3% of those from venezuelan patients. all possible combinations of vaca regions were found, with the exception of s2/m1. the predominant combination found in both countries was s1/m1. the percentage of caga+ strains was increased by the use of a second set of primers and a greater number of strains was amplified with the b7629/b7628 primers in the cuban patients (p = 0.0001). there was no significant difference between the presence of the allelic variants of vaca and caga in both populations. the predominant genotype was caga+/s1m1 in both countries. the results support the necessary investigation of isolates circulating among the human population in each region.
CagA status and VacA subtypes of Helicobacter pylori in relation to histopathologic findings in Iranian population  [cached]
Molaei Mahsa,Foroughi Forough,Mashayekhi Reza,Haghazali Mehrdad
Indian Journal of Pathology and Microbiology , 2010,
Abstract: Background/Objective: The aim of this study was to detect dominant cagA/vacA genotypes of Helicobacter Pylori (H. pylori) and determine correlations between different cagA/vacA genotypes and histologic features of chronic gastritis in Iranian patients. Methods: Gastric biopsy was taken from 166 patients with nonulcer dyspepsia. The specimens were processed and DNA from each H. pylori isolate was extracted from multiple colony sweeps for identification of glmM gene. The vacA subtypes and cagA gene were tested by PCR . Histopathological features were recorded and graded according to partial Sydney system. Results: Of the 86 strains, 66 (76.7%) were cagA positive. The proportions of vacA gene subtypes s1, s2, m1 and m2 in the 78 strains isolated were 70.5%, 29.5%, 37.2% and 62.8%, respectively. About 83.3% of the vacA-positive strains had s1 allele. Twenty-six strains (33.3%) were positive for both cagA and m1 allele. Positive cagA status and vacA subtypes were not associated significantly with presence of neutrophil infiltration, intestinal metaplasia or H. pylori density. Only vacA s1 was significantly associated with more severe inflammation (P=0.02). The dominant genotype of H. pylori was vacA plus s1/m2. CagA gene positivity rate was not closely associated with severity of the disease. Conclusion: H. pylori strains showing vacA s1 genotype were associated with more severe gastritis. These findings show that vacA genotyping may have clinical relevance in Iran.
Clinical and pathological importance of vacA allele heterogeneity and cagA status in peptic ulcer disease in patients from North Brazil
Martins, Luisa Caricio;Corvelo, Tereza Cristina de Oliveira;Demachki, Samia;Araujo, Marialva TF;Assump??o, M?nica Baraúna;Vilar, Simone Cristina Araujo Jucá;Freitas, Felipe Bonfim;Barbosa, Hivana Patricia Melo;Fecury, Amanda Alves;Amaral, Renata Kelly Costa do;Santos, Sidney Emanuel Batista dos;
Memórias do Instituto Oswaldo Cruz , 2005, DOI: 10.1590/S0074-02762005000800009
Abstract: we have examined the prevalence of gene caga and vaca alleles in 129 patients, 69 with gastritis and 60 with peptic ulcer diseases from north brazil and their relation with histopathological data. vaca and caga genotype were determined by polymerase chain reaction. hematoxylin-eosin staining was used for histological diagnosis. 96.6% of the patients were colonized by helicobacter pylori strains harboring single vaca genotype (nont-mixed infection). among them, 11.8% had subtype s1a, 67.8% had subtype s1b, and 17% subtype s2. in regard to the middle region analysis, m1 alleles were found in 75.4% and m2 in 21.2% of patients. the caga gene was detected in 78% patients infected with h. pylori and was associated with the s1-m1 vaca genotype. the h. pylori strains, vaca s1b m1/caga-positive, were associated with increased risk of peptic ulcer disease and higher amounts of lymphocytic and neutrophilic infiltrates and the presence of intestinal metaplasia. these findings show that caga and vaca genotyping may have clinical relevance in brazil.
Prevalence of Helicobacter pylori vacA, cagA, dupA and oipA Genotypes in Patients with Gastric Disease  [PDF]
Mayara Luciana Sallas, Jessica Lima Melchiades, Luanna Munhoz Zabaglia, Juliana Ribeiro do Prado Moreno, Wilson Aparecido Orcini, Elizabeth Suchi Chen, Marilia de Arruda Cardoso Smith, Spencer Luiz Marques Pay?o, Lucas Trevizani Rasmussen
Advances in Microbiology (AiM) , 2017, DOI: 10.4236/aim.2017.71001
Abstract: Gastric diseases such as chronic gastritis and gastric cancer are most commonly caused by virulence factors of Helicobacter pylori (H. pylori), such as the vacA, cagA, dupA and oipA genes. Therefore, this study investigated the prevalence and the combination of these virulence factors from patients with gastric diseases. The endoscopic biopsies were obtained from 516 patients with gastric symptoms, 101 of which were from patients with normal gastric tissue, 365 of which were from patients with chronic gastritis, and 50 of which were from patients with gastric cancer. H. pylori and the virulence factors were detected by PCR. The oipA gene exhibited an increased risk for chronic gastritis (p = 0.0296), and the vacA gene demonstrated a risk for gastric cancer from chronic gastritis (p = 0.0002). Based on the combination of the virulence factors, cagA, vacA, dupA and oipA genes exhibited a high prevalence in patients with chronic gastritis and gastric cancer. The cagA+/dupA+ genotype demonstrated a significant correlation in patients with normal gastric mucosa (p = 0.0278). In the chronic gastritis group, a significant association was observed between the cagA+ and the vacA s1m1 genotypes (p < 0.0001), the cagA+/dupA+ genotypes (p = 0.0183), the dupA+/oipA+ genotypes (p < 0.0001), and the dupA+/vacA s1m1 genotypes (p = 0.0008) genotypes. This study revealed a high prevalence of the combination of cagA, vacA, dupA, and oipA genes, which contributed to the risk of developing gastroduodenal diseases. Furthermore, this is the first study to reveal a high prevalence of the oipA gene in H. pylori isolates in Brazil.
Prevalence of Helicobacter pylori vacA, cagA, iceA and oipA genotypes in Tunisian patients
Khansa Ben Mansour, Chédlia Fendri, Meriem Zribi, Afef Masmoudi, Mounir Labbene, Azza Fillali, Nabil Ben Mami, Taoufik Najjar, Ahmed Meherzi, Tahar Sfar, Christophe Burucoa
Annals of Clinical Microbiology and Antimicrobials , 2010, DOI: 10.1186/1476-0711-9-10
Abstract: H. pylori was cultured from endoscopic biopsies obtained from 281 Tunisian patients. The vacA alleles, cagA, iceA and oipA genotypes were determined by PCR.The vacA s1m1, s1m2 and s2m2 were respectively found in 10.7%, 12.5% and 45.6% of strains. The s2m1 genotype was not detected in our study. The cagA was found in 61.6% of isolates. The iceA1 and the iceA2 genotypes were respectively isolated in 60.2% and in 16% of strains. The oipA genotype was detected in 90.8% of strains. Considering the vacA and iceA genotypes, the presence of multiple H. pylori strains in a single biopsy specimen was found respectively in 31.4% and 23.8%. The comparison between strains isolated from antrum and fundus showed that Tunisian patients were infected with two or more strains of different cagA, vacA, iceA and oipA genotypes and the discordance was respectively in 9.6%, 4.6%, 8.9% and 8.5% of strains.Our results showed that in 46% (131 strains among 281), the H. pylori strains were highly virulent in relation of the three or four virulent factors they could carry. These finding were described before in the literature. Tunisian patients were colonized by one or multiple strains of H. pylori in the same time in relation of presence of vacA m1/m2 and iceA1/iceA2 in the same biopsy. The discordance between strains isolated from antrum and fundus was high, and it is in favour of multicolonization.Helicobacter pylori (H. pylori) is one of the most common bacterial pathogens of humans and has a worldwide distribution. Infection by H. pylori is associated with the development of chronic gastritis, gastric or duodenal ulcer, gastric cancer and MALT-lymphoma [1]. Different virulence genes have been described in H. pylori infection such as cagA, vacA, iceA and oipA genes. The cytotoxin-associated gene (cagA) is frequently associated with cytotoxin production and the induction of interleukin 8 (IL8) by gastric epithelial cells [2]. Several studies have suggested that cagA is a useful marker for t
cagA and vacA in strains of Helicobacter pylori from ulcer and non-ulcerative dyspepsia patients
Gustavo Faundez, Miriam Troncoso, Guillermo Figueroa
BMC Gastroenterology , 2002, DOI: 10.1186/1471-230x-2-20
Abstract: 38 strains were isolated from patients with non-ulcerative dyspepsia (NUD) and 25 were isolated from colonized individuals with peptic ulcers. The genotypic characterization was carried out utilizing PCR methodology. The presence of the cagA gene was detected using two set of primers from the middle conservative region of the cagA, and primers for the signal and middle region were used for the genotyping of vacAThe presence of cagA showed similar rates in strains from peptic ulcers (60%) and NUD patients (55%). Also similar was the prevalence of the allelic form s1 of vacA between the strains obtained from ulcers or NUD patients. However, the combination cagA+/vacA s1m1 was found more frequently among the H. pylori strains from peptic ulcer patients (52%) than among strains isolated from NUD patients (26%), this difference was statistically significant (p = 0.035).The presence of either cagA or the allelic variant s1 vacA alone do not have a predictive value as as a risk markers of severe gastric pathologies in the Chilean population. However, being infected by a H. pylori strain with the genotype cagA+/vacA s1m1 may be associated to an increased risk of acquiring a peptic ulcer disease.Helicobacter pylori infects about half of the world population, but only a reduced percentage develops peptic ulcers or gastric cancer, both conditions are strongly related with H. pylori infection in Chile [1]. It has been suggested that patients with severe gastroduodenal symptoms are infected with more virulent strains of H. pylori, while those individuals that just develop gastritis are infected with strains of low pathogenic potential. cagA is one of the markers for a pathogenicity island of ca. 40 kilobases, which has been associated to more severe clinical outcomes [2]. vacA codes for another important virulence factor that induces vacuolization on eukaryotic cells in vitro, and different allelic variants in two regions of this gene has been described. The N-terminal signal re
High Diversity of vacA and cagA Helicobacter pylori Genotypes in Patients with and without Gastric Cancer  [PDF]
Yolanda López-Vidal, Sergio Ponce-de-León, Gonzalo Castillo-Rojas, Rafael Barreto-Zú?iga, Aldo Torre-Delgadillo
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003849
Abstract: Background Helicobacter pylori is associated with chronic gastritis, peptic ulcers, and gastric cancer. The aim of this study was to assess the topographical distribution of H. pylori in the stomach as well as the vacA and cagA genotypes in patients with and without gastric cancer. Methodology/Principal Findings Three gastric biopsies, from predetermined regions, were evaluated in 16 patients with gastric cancer and 14 patients with dyspeptic symptoms. From cancer patients, additional biopsy specimens were obtained from tumor centers and margins; among these samples, the presence of H. pylori vacA and cagA genotypes was evaluated. Positive H. pylori was 38% and 26% in biopsies obtained from the gastric cancer and non-cancer groups, respectively (p = 0.008), and 36% in tumor sites. In cancer patients, we found a preferential distribution of H. pylori in the fundus and corpus, whereas, in the non-cancer group, the distribution was uniform (p = 0.003). A majority of the biopsies were simultaneously cagA gene-positive and -negative. The fundus and corpus demonstrated a higher positivity rate for the cagA gene in the non-cancer group (p = 0.036). A mixture of cagA gene sizes was also significantly more frequent in this group (p = 0.003). Ninety-two percent of all the subjects showed more than one vacA gene genotype; s1b and m1 vacA genotypes were predominantly found in the gastric cancer group. The highest vacA-genotype signal-sequence diversity was found in the corpus and 5 cm from tumor margins. Conclusion/Significance High H. pylori colonization diversity, along with the cagA gene, was found predominantly in the fundus and corpus of patients with gastric cancer. The genotype diversity observed across systematic whole-organ and tumor sampling was remarkable. We find that there is insufficient evidence to support the association of one isolate with a specific disease, due to the multistrain nature of H. pylori infection shown in this work.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.