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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.
Expression of AQP3 gene in chronic atrophic and chronic superficial gastritis patients  [cached]
Shijun Zhang,Genxin Chen,Ying Peng Cui,Shaoxian Lao
Journal of Research in Medical Sciences , 2007,
Abstract: BACKGROUND: Most studies about aquaporin 3 (AQP3) in the gastrointestinal tract were carried out on both in vivo and in vitro. The role of AQP3-mediated water transport in human gastrointestinal tract is still unclear. Our aim in this study was to explore the expression of AQP3 gene in chronic atrophic gastritis (CAG) and chronic superficial gastritis (CSG) atients and to determine its possible function in the development of gastritis. METHODS: Twenty-two outpatients diagnosed as CSG and 12 outpatients diagnosed as CAG were selected randomly. Ten cases of healthy individuals were selected as normal control group. In all cases, AQP3 gene expression of gastric mucosa was detected by fluorescence quantitative polymerase chain reaction (FQ-PCR). RESULTS: The AQP3 gene expression was significantly higher in gastric mucosa of CSG and healthy individuals than that in CAG (P<0.01). However, there was no significant difference in the AQP3 gene expression between helicobacter pylori positive patients and helicobacter pylori negative patients (P>0.05). CONCLUSIONS: AQP3 expression might play certain role in the occurrence and development of gastritis. KEY WORDS: Aquaporin 3, chronic superficial gastritis, chronic atrophic gastritis.
Risk for gastric neoplasias in patients with chronic atrophic gastritis: A critical reappraisal  [cached]
Lucy Vannella,Edith Lahner,Bruno Annibale
World Journal of Gastroenterology , 2012, DOI: 10.3748/wjg.v18.i12.1279
Abstract: Chronic atrophic gastritis (CAG) is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue (non-metaplastic atrophy) or by glandular structures inappropriate for location (metaplastic atrophy). Epidemiological data suggest that CAG is associated with two different types of tumors: Intestinal-type gastric cancer (GC) and type I gastric carcinoid (TIGC). The pathophysiological mechanisms which lead to the development of these gastric tumors are different. It is accepted that a multistep process initiating from Helicobacter pylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The TIGC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of TIGC. Thus, several events occur in the gastric mucosa before the development of intestinal-type GC and/or TIGC and these take several years. Knowledge of CAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors associated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias.
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.
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.
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
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.
Broccoli consumption and chronic atrophic gastritis among Japanese males: an epidemiological investigation.
Sato K,Kawakami N,Ohtsu T,Tsutsumi A
Acta Medica Okayama , 2004,
Abstract: Previous in vitro and animal experiments have shown that sulforaphane, which is abundant in broccoli, inhibits Helicobacter pylori (H. pylori) infection and blocks gastric tumor formation. This suggests that broccoli consumption prevents chronic atrophic gastritis (CAG) introduced by H. pylori infection and, therefore, gastric cancer. For an epidemiological investigation of the relationship between the broccoli consumption and CAG, a cross-sectional study of 438 male employees, aged 39 to 60 years, of a Japanese steel company was conducted. CAG was serologically determined with serum cut-off values set at pepsinogen I < or = 70 ng/ml and a ratio of serum pepsinogen I/pepsinogen II < or = 3.0. Broccoli consumption (weekly frequency) and diet were monitored by using a 31-item food frequency questionnaire. The prevalence of CAG among men who ate broccoli once or more weekly was twice as high as that among men who consumed a negligible amount (P < 0.05). Multiple logistic regression analysis indicated that broccoli consumption once or more weekly significantly increased the risk for CAG (odds ratio, 3.06; 95% confidence interval, 1.12-8.38; P < 0.05), after controlling for age, education, cigarette smoking, and alcohol consumption. The present study failed to show an expected association between frequent broccoli consumption and a low prevalence of CAG.
DNA repair gene polymorphisms and risk of chronic atrophic gastritis: a case-control study
Bernd Frank, Heiko Müller, Melanie Weck, Norman Klopp, Thomas Illig, Elke Raum, Hermann Brenner
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-440
Abstract: A nested case-control study within the German population-based ESTHER cohort was conducted, including 533 CAG cases and 1054 controls. Polymorphisms in eleven DNA repair genes (APEX1, ERCC1, ERCC2/XPD, PARP1 and XRCC1), in CD3EAP/ASE-1 and PPP1R13L were analysed.No association was disclosed for any of the analysed polymorphisms. Nor did stratified analyses according to ages < 65 and ≥ 65 years show any significant association with CAG risk.The results of this large German case-control study do not reveal associations of DNA repair pathway polymorphisms and risk of CAG. On the basis of a large number of CAG cases, they do not support associations of DNA repair pathway SNPs with CAG risk, but suggest the need of larger studies to disclose or exclude potential weak associations, or of studies with full coverage of candidate genes.Chronic atrophic gastritis (CAG) is a well-established precursor lesion in the aetiology of intestinal gastric cancer (GC), the most common type of GC [1]. Unlike the diffuse type of gastric carcinoma, a recent steady decline in incidence has been observed for the intestinal type [1,2]. Several changes have been identified as precursors to the intestinal type of gastric carcinoma, representing sequential steps in the precancerous process: non-atrophic gastritis, CAG (gland loss), metaplasia and dysplasia [1]. This progression usually takes decades, providing excellent options for timely detection and intervention at precancerous stages [1,3]. The multistage model of gastric carcinoma development assumes that carcinogenesis is initiated by host-inflammatory response following infection by the Gram-negative bacterium Helicobacter pylori (H. pylori), and by dietary exposure to salt and nitrate, which cause DNA damage [4-7]. To date, three molecular mechanisms, by which H. pylori may provoke a loss of genomic integrity and promote transformation, are postulated [6,7]. These include a) mutations in mitochondrial DNA, b) the induction of a transient
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