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Genotipo cag A+ en cepas de Helicobacter pylori asociadas a úlcera péptica, gastritis crónica y cáncer gástrico
Martínez Echavarría,María Teresa; González Torres,Maximino; Ferreira Capote,Raúl; Mas Páez,Juan Antonio;
Revista Cubana de Medicina , 2008,
Abstract: abstract 171 patients with duodenal ulcer, gastric ulcer, chronic gastritis and gastric cancer were studied. the last 3 were histologically confirmed. 56 cases with duodenal ulcer, 48 with gastric ulcer, 47 with chronic gastritis and 20 with gastric cancer were analyzed. the presence of helicobacter pylori was detected by pcr in 98.2 % of the duodenal ulcers; in 95.8 % of the gastric ulcers; in 95.0 % of the gastric cancers; and in 93.6 % of the chronic gastritis. the cag a genotyping of the strains found proved to be positive in 80.0 % of the duodenal ulcers; in 72.7 % of the chronic gastritis; in 69.6 % of the gastric ulcers; and in 42.1 % of the gastric cancers, for a total prevalence of 70.7 %. both, the ulcers as a whole and the chronic gastritis showed a prevalence of cag a+ strains of helicobacter pylori significantly higher than gastric cancer (p = 0,19).
Conserved Transcriptional Unit Organization of the Cag Pathogenicity Island among Helicobacter pylori Strains  [PDF]
Olga Shiva,Karen M. Ottemann,Andrea R. Castillo,Jay V. Solnick
Frontiers in Cellular and Infection Microbiology , 2012, DOI: 10.3389/fcimb.2012.00046
Abstract: The Helicobacter pylori cag pathogenicity island (cag PAI) encodes a type IV secretion system that is more commonly found in strains isolated from patients with gastroduodenal disease than from those with asymptomatic gastritis. Genome-wide organization of the transcriptional units in H. pylori strain 26695 was recently established using RNA sequence analysis (Sharma et al., 2010). Here we used quantitative reverse-transcription polymerase chain reaction of open reading frames and intergenic regions to identify putative cag PAI operons in H. pylori; these operons were analyzed further by transcript profiling after deletion of selected promoter regions. Additionally, we used a promoter-trap system to identify functional cag PAI promoters. The results demonstrated that expression of genes on the H. pylori cag PAI varies by nearly five orders of magnitude and that the organization of cag PAI genes into transcriptional units is conserved among several H. pylori strains, including, 26695, J99, G27, and J166. We found evidence for 20 transcripts within the cag PAI, many of which likely overlap. Our data suggests that there are at least 11 operons: cag1-4, cag3-4, cag10-9, cag8-7, cag6-5, cag11-12, cag16-17, cag19-18, cag21-20, cag23-22, and cag25-24, as well as five monocistronic genes (cag4, cag13, cag14, cag15, and cag26). Additionally, the location of four of our functionally identified promoters suggests they are directing expression of, in one case, a truncated version of cag26 and in the other three, transcripts that are antisense to cag7, cag17, and cag23. We verified expression of two of these antisense transcripts, those antisense to cag17 and cag23, by reverse-transcription polymerase chain reaction. Taken together, our results suggest that the cag PAI transcriptional profile is generally conserved among H. pylori strains, 26695, J99, G27, and J166, and is likely complex.
The Prevalence of Helicobacter pylori Infection Decreases with Older Age in Atrophic Gastritis  [PDF]
Shaohua Chen,Lixiong Ying,Mei Kong,Yu Zhang,Youming Li
Gastroenterology Research and Practice , 2013, DOI: 10.1155/2013/494783
Abstract: The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however, H. pylori positivity and inflammatory activity decreased significantly with increased age. H. pylori infection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects with H. pylori infection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence of H. pylori infection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG. 1. Introduction Chronic atrophic gastritis (CAG) is a histopathologic entity characterized by chronic inflammation of the gastric mucosa with loss of gastric glandular cells. CAG, intestinal metaplasia (IM), and epithelial dysplasia (ED) of the stomach are common and are associated with an increased risk of gastric cancer. CAG and IM are considered to be precancerous conditions. ED represents the penultimate stage of the gastric carcinogenesis sequence, defined as histologically unequivocal neoplastic epithelium without evidence of tissue invasion, and is thus a direct neoplastic precancerous lesion. ED is characterized by cellular atypia reflective of abnormal differentiation and disorganized glandular architecture. Helicobacter pylori are Gram-negative bacteria that colonize the human gastric epithelium and represent one of the most common human infections worldwide. H. pylori infection is usually contracted in the first few years of life, and its prevalence increases with older age and lower socioeconomic status during childhood [1]. This infection is the primary inducer of CAG, IM, and ED. More than half of all humans have H. pylori colonies in their stomachs; however, only a minority of H. pylori-infected individuals develop cancer of the stomach [2]. Haziri et al. [3] reported that the prevalence of H. pylori infection was high in patients with CAG (66.0%), IM (71.7%), and gastric dysplasia (71.4%). In the present study, the clinical and histopathological characteristics of 3969 CAG patients from our hospital were retrospectively studied, and the relationship
Clinical significance of infection with cag A and vac A positive helicobacter pylori strains  [PDF]
Soki?-Milutinovi? Aleksandra,Todorovi? Vera N.,Milosavljevi? Tomica
Srpski Arhiv za Celokupno Lekarstvo , 2004, DOI: 10.2298/sarh0412458s
Abstract: Clinical relevance of infection with different Helicobacter pylori strains was reviewed in this paper. Helicobacter pylori (H. pylori) infection plays a role in pathogenesis of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma. Extragastric manifestations of H. pylori infection most probably include acne rosacea and chronic urticaria, while the importance of H. pylori infection for pathogenesis of growth retardation in children, iron deficiency anemia, coronary heart disease, stroke and idiopathic thrombocytopenic purpura remains vague. The expression of two H. pylori proteins, cytotoxin associated protein (cag A) and vacuolization cytotoxin (vac A) is considered to be related with pathogenicity of the bacterium. It is clear that presence of cag A+ strains is important for development of peptic ulcer; nevertheless, it is also protective against esophageal reflux disease. On the other hand, cag A+ strains are common in gastric adenocarcinoma and MALT lymphoma patients, but it seems that certain subtypes of vac A cytotoxin are more important risk factors. Infection with cag A+ strains is more common in patients with acne rosacea, stroke and coronary heart disease.
Presence of the Genes cagA, cagE, virB11 and Allelic Variation of vacA of Helicobacter pylori Are Associated with the Activity of Gastritis  [PDF]
Pedro Pinheiro de Negreiros Bessa, Francivandi Coelho Barbosa, Ana Paula Santos do Carmo, Gildo Barreira Furtado, Fernanda Capelo Barroso, Silvia Helena Barem Rabenhosrt
Open Journal of Gastroenterology (OJGas) , 2014, DOI: 10.4236/ojgas.2014.411049
Abstract: Non-atrophic active chronic gastritis (ACG) is characterized by the presence of H. pylori in the gastric epithelium, known to be one of the first steps that precede progression to gastric adenocarcinoma. Inactive chronic gastritis (ICG) suggests that the patient has H. pylori gastritis, but this diagnosis is rarely made in routine histopathology. Clinical manifestations associated with H. pylori infection are potentially due to differences in virulence between strains; however, it is unclear if the progression of ACG to ICG depends on the H. pylori strain. The aim of this study was to compare the prevalence of the virulence factors of H. pylori found in patients with ACG and ICG, and its influence on the development of ICG. A significant association was observed between H. pylori detection by histological examination and the activity of gastritis (p < 0.01). Long-term use of proton pump inhibitors (PPI) (>1 year) was reported by 28.6% of the ACG group and 42.5% of the ICG, while no evidence of association between long-term use of PPI and decreased inflammation was found in the patients studied. The genes cagA, cagE and virB11 were statistically associated with ACG (p = 0.01, p < 0.001 and p = 0.002, respectively). In the vacAs1 allele groups, ACG was associated with the most virulent group (p = 0.0015), while ICG was associated with the less virulent group (p < 0.001). The rate of co-infection was significantly higher in ICG than in ACG cases (p = 0.02). In conclusion, this study points to the role of virulent strains of H. pylori in the non-resolution of gastritis.
The type IV secretion system encoded by the cag PAI of Helicobacter pylori]
幽门螺杆菌cag PAI编码的Ⅳ型分泌系统

CUI Lei-lei,SHAO Shi-he,
崔蕾蕾
,邵世和

微生物学报 , 2007,
Abstract: Helicobacter pylori is a human-specific gastric pathogen that colonizes over half the world's population. Infection with this bacterium is associated with a spectrum of gastric pathologies ranging from mild gastritis to peptic ulcers and gastric cancer. A strong predictor of severe disease outcome is infection with a bacterial strain harbouring the cag (cytotoxin associated gene) pathogenicity island (PAI), a 40 kb stretch of DNA that encodes homologues of several components of a type IV secretion system (TFSS). One gene within the cag PAI, cagA, has been shown to encode a substrate for the TFSS which is translocated into host cells, inducing the dephosphrylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. It appeears to play a key role in H. pylori pathogenesis. Very little is known about the H. pylori cag PAI-encoded TFSS, the expression of Cag proteins in H. pylori, and the functions of individual proteins encoded by the cag PAI. Only by exploring the mechanistic details of the interplay between H. pylori and eukaryotic cells can we endeavour to understand how these cellular interactions play out at the tissue and organismal level during the lifelong coexistence of bacterium and host.
Prevalence of Helicobacter pylori cagA and sabA Genotypes in Patients with Gastric Disease  [PDF]
Jéssica Nunes Pereira, Wilson A. Orcini, Rita L. Peruquetti, Marilia A. C. Smith, Spencer L. M. Pay?o, Lucas T. Rasmussen
Advances in Microbiology (AiM) , 2019, DOI: 10.4236/aim.2019.93017
Abstract: Gastric cancer is one of the most common types of cancer worldwide. Helicobacter pylori is considered one of the most important causes of this condition specially because of its virulence markers as sabA and cagA. Therefore, we aim to investigate the relation between these markers and the gastric diseases in 400 patients who underwent upper digestive endoscopy. To detect the bacteria and its genes by Polymerase Chain Reaction (PCR), the presence of H. pylori was significant when comparing the groups control vs. cancer (p value < 0.0001) OR [95% CI] 12.73 (5.45 - 29.69) and the groups control vs. chronic gastritis (p value < 0.0001) OR [95% CI] 12.99 (7.44 - 22.66). cagA was statistically significant considering its presence when comparing the chronic gastritis vs. cancer groups (p value = 0.0434) OR [95% CI] 2.44 (1.021 - 5.845). Associating both sabA and cagA, we found a statistically significant result (p value < 0.0001) OR [95% CI] 13.68 (3.95 - 47.33) considering the gastritis vs. cancer groups. Helicobacter pylori is directly associated to gastric diseases such as gastritis and cancer and its virulence markers: sabA and cagA increase the injury process to the gastric epithelium making the host more susceptible to cancer.
Nodular gastritis and Helicobacter pylori infection in childhood
. Kostaki Maria, Fessatou Smaragdi, Karpathios Th.
Annals of Gastroenterology , 2007,
Abstract: Helicobacter pylori (HP) associated gastritis and peptic ulcer have been initially reported in adult patients. Recently, this association has also been demonstrated in children. We investigated 18 children (8-14 years old) with recurrent abdominal pain. In 7 patients gastroduodenoscopy revealed gastritis and HP was identified. Giemsa stain was more sensitive than urease testing in identifying the bacteria. In 5 of the 7, a nodular appearance of the antral mucosa was observed. The histological examination suggests lymphoid hyperplasia as the cause of the nodularity. All 7 patients became symptomless after a triple therapy with omeprazole, clarithromycin and amoxycillin for 2 weeks. We conclude that nodular gastritis is a peculiar type of gastritis in children. It is frequently found in association with HP infection. Two weeks triple therapy is an effective treatment in children with HP infection. Key words: Helicobacter pylori, nodular gastritis, peptic ulcer disease, childhood
Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils  [PDF]
Tobias Wiedemann, Eva Loell, Susanna Mueller, Mechthild Stoeckelhuber, Manfred Stolte, Rainer Haas, Gabriele Rieder
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004754
Abstract: Infection with Helicobacter pylori, carrying a functional cag type IV secretion system (cag-T4SS) to inject the Cytotoxin associated antigen (CagA) into gastric cells, is associated with an increased risk for severe gastric diseases in humans. Here we studied the pathomechanism of H. pylori and the role of the cag-pathogenicity island (cag-PAI) for the induction of gastric ulcer and precancerous conditions over time (2–64 weeks) using the Mongolian gerbil model. Animals were challenged with H. pylori B128 (WT), or an isogenic B128ΔcagY mutant-strain that produces CagA, but is unable to translocate it into gastric cells. H. pylori colonization density was quantified in antrum and corpus mucosa separately. Paraffin sections were graded for inflammation and histological changes verified by immunohistochemistry. Physiological and inflammatory markers were quantitated by RIA and RT-PCR, respectively. An early cag-T4SS-dependent inflammation of the corpus mucosa (4–8 weeks) occurred only in WT-infected animals, resulting in a severe active and chronic gastritis with a significant increase of proinflammatory cytokines, mucous gland metaplasia, and atrophy of the parietal cells. At late time points only WT-infected animals developed hypochlorhydria and hypergastrinemia in parallel to gastric ulcers, gastritis cystica profunda, and focal dysplasia. The early cag-PAI-dependent immunological response triggers later physiological and histopathological alterations towards gastric malignancies.
Evaluation of the Pattern of EPIYA Motifs in the Helicobacter pylori cagA Gene of Patients with Gastritis and Gastric Adenocarcinoma from the Brazilian Amazon Region  [PDF]
Adenielson Vilar e Silva,Mario Ribeiro da Silva Junior,Ruth Maria Dias Ferreira Vinagre,Kemper Nunes Santos,Renata Aparecida Andrade da Costa,Amanda Alves Fecury,Juarez Ant?nio Sim?es Quaresma,Luisa Caricio Martins
International Journal of Bacteriology , 2014, DOI: 10.1155/2014/418063
Abstract: The Helicobacter pylori is associated with the development of different diseases. The clinical outcome of infection may be associated with the cagA bacterial genotype. The aim of this study was to determine the EPIYA patterns of strains isolated from patients with gastritis and gastric adenocarcinoma and correlate these patterns with the histopathological features. Gastric biopsy samples were selected from 384 patients infected with H. pylori, including 194 with chronic gastritis and 190 with gastric adenocarcinoma. The presence of the cagA gene and the EPIYA motif was determined by PCR. The cagA gene was more prevalent in patients with gastric cancer and was associated with a higher degree of inflammation, neutrophil activity, and development of intestinal metaplasia. The number of EPIYA-C repeats showed a significant association with an increased risk of gastric carcinoma (OR = 3.79, 95% CI = 1.92–7.46, and ). A larger number of EPIYA-C motifs were also associated with intestinal metaplasia. In the present study, infection with H. pylori strains harboring more than one EPIYA-C motif in the cagA gene was associated with the development of intestinal metaplasia and gastric adenocarcinoma but not with neutrophil activity or degree of inflammation. 1. Introduction Helicobacter pylori is a spiral Gram-negative bacterium that infects the stomach and causes chronic gastritis. In addition, the bacterium plays an important role in the pathogenesis of gastroduodenal ulcer and gastric carcinoma [1]. The diverse clinical outcomes of H. pylori infection depend on factors such as bacterial virulence, host susceptibility, and environmental factors [2]. Protein-associated gene A (CagA) is an important virulence factor of H. pylori that is found in 70 to 80% of strains isolated in Brazilian cities and is associated with the development of peptic ulcers and gastric carcinoma [3, 4]. This protein is encoded by the cagA gene, which is located on the cag pathogenicity island (cag-PAI). After adhesion of cagA-positive H. pylori strains to the gastric epithelium, the CagA protein is injected directly into the host cell through a type IV secretion system encoded by the cag-PAI. Inside the epithelial cell, CagA is phosphorylated in its carboxy-terminal region. This region is highly variable and contains a polymorphic pattern of Glu-Pro-Ile-Tyr-Ala amino acid repeats (EPIYA motif) [5, 6]. Four types of EPIYA segments have been described (EPIYA-A, -B, -C, and -D) [7, 8]. CagA proteins always possess the EPIYA-A and EPIYA-B sites, but some proteins also contain one or more
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