The relationship between H. pylori virulence genotypes and gastric diseases

Tumor Etiology and Screening Department of Cancer Institute and General Surgery, First Affiliated Hospital of China Medical University, Key Laboratory of Cancer Control, Liaoning Province, Shenyang, China.
Polish journal of microbiology / Polskie Towarzystwo Mikrobiologów = The Polish Society of Microbiologists (Impact Factor: 0.7). 11/2012; 61(2):147-50.
Source: PubMed


There have been no reports on the relationship between virulence genes and gastric diseases based on the same bacterial colonization density. Our results indicated that Helicobacter pylori virulence genes were more relevant than colonization density as a pathogenic mechanism of gastric diseases, which helps elucidate the pathogenic mechanisms of bacteria and aids in the development of improved strategies for the treatment of gastric disease.

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    • "Helicobacter pylori is a gram-negative bacterium that colonizes the gastric antrum and/or the body of the human stomach, causing complications such as gastritis, gastric and duodenal ulcer and gastric malignancies [1,2]. H. pylori is present in approximately half of the world population [3]. "
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    ABSTRACT: Epidemiological investigations have indicated that Helicobacter pylori induces inflammation in the gastric mucosa regulated by several interleukins. The genes IL1B and IL8 are suggested as key factors in determining the risk of gastritis. The aim of this paper was to evaluate the association of gene polymorphism of interleukin-1 and interleukin-8 with chronic gastrits in H. pylori infected patients. A total of 60 patients underwent endoscopic procedure. Biopsy samples were collected for urease test, histopathological and molecular exams. The DNA of theses samples was extracted for detection of H. pylori and analysis of the genes mentioned above. Patients with gastritis had a higher frequency of H. pylori-positive samples. H. pylori was detected in 30/60 patients (50%) by PCR. As for polymorphism of interleukin 8 (-251) gene we observed a statistical difference when analyzed TA (p = 0.039) and TT (p = 0.047) genotypes. In the IL1B31 there was a statistical difference in TT (p = 0.01) genotype and in the IL1B-511 there wasn't any statistical difference. Our results suggest a strong correlation between the presence of chronic gastritis and infection by H. pylori and that IL1B-31TT and IL8-251TT genotypes appear to act as protective factors against H. pylori infection while IL8-251TA genotype may comprise a risk factor for infection with this bacterium.
    Journal of Venomous Animals and Toxins including Tropical Diseases 04/2014; 20(1):17. DOI:10.1186/1678-9199-20-17 · 0.80 Impact Factor
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    • "Helicobacter pylori is a gram-negative spiral bacterium that colonizes the human stomach. It is estimated that approximately half of the world’s population is infected with it [1,2]. In 1994, the International Agency for Research on Cancer included H. pylori infection in group I carcinogens. "
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    ABSTRACT: Only a few Helicobacter pylori-infected individuals develop severe gastric diseases and virulence factors of H. pylori appear to be involved in such clinical outcomes. Duodenal ulcer promoting gene A (dupA) is a novel virulence factor of Helicobacter pylori that is associated with duodenal ulcer development and reduced risk for gastric carcinoma in some populations. The aims of the present study were to determine the presence of dupA gene and evaluate the association among dupA and other virulence factors including cagA and vacA in Brazilian patients. Gastric biopsies were obtained from 205 dyspeptic patients (100 children and 105 adults). DNA was extracted and analyzed for the presence of H. pylori and its virulence factors using the polymerase chain reaction method. Patients with gastritis tested positive for H. pylori more frequently. The dupA gene was detected in 41.5% of them (85/205); cagA gene was found in 98 isolates (47.8%) and vacA genotype s1/m1 in 50.2%, s1/m2 in 8.3%, s2/m2 in 36.6%, s2/m1 in 0.5% and s1/s2/m1/m2 in 4.4%. We also verified a significant association between cagA and dupA genes [p = 0.0003, relative risk (RR) 1.73 and confidence interval [CI] = 1.3-2.3]. The genotypes s1/m1 were also associated with dupA gene (p = 0.0001, RR: 1.72 and CI: 1.3-2.2). The same associations were found when analyzing pediatric and adult groups of patients individually. Ours results suggest that dupA is highly frequent in Brazilian patients and is associated with cagA gene and vacA s1/m1 genotype, and it may be considered an important virulence factor in the development of gastric diseases in adults or children.
    Journal of Venomous Animals and Toxins including Tropical Diseases 01/2014; 20(1):1. DOI:10.1186/1678-9199-20-1 · 0.80 Impact Factor
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    ABSTRACT: Helicobacter pylori (H. pylori) is a pathogen and the most frequent cause of gastric ulcers. There is also a close correlation between the prevalence of H. pylori infection and the incidence of gastric cancer. We present the case of a 38-year-old woman referred by her primary care physician for screening positron emission tomography-computed tomography (PET-CT), which showed a nodular strong accumulation point with standardized uptake value 5.6 in the gastric fundus. Gastroscopy was then performed, and a single arched ulcer, 12 mm in size, was found in the gastric fundus. Histopathological examination of the lesion revealed chronic mucosal inflammation with acute inflammation and H. pylori infection. There was an obvious mitotic phase with widespread lymphoma. Formal anti-H. pylori treatment was carried out. One month later, a gastroscopy showed a single arched ulcer, measuring 10 mm in size in the gastric fundus. Histopathological examination revealed chronic mucosal inflammation with acute inflammation and a very small amount of H. pylori infection. The mitotic phase was 4/10 high power field, with some heterotypes and an obvious nucleolus. Follow-up gastroscopy 2 mo later showed the gastric ulcer in stage S2. The mucosal swelling had markedly improved. The patient remained asymptomatic, and a follow-up PET-CT was performed 6 mo later. The nodular strong accumulation point had disappeared. Follow-up gastroscopy showed no evidence of malignant cancer. H. pylori-associated severe inflammation can lead to neoplastic changes in histiocytes. This underscores the importance of eradicating H. pylori, especially in those with mucosal lesions, and ensuring proper follow-up to prevent or even reverse early gastric cancer.
    World Journal of Gastroenterology 03/2013; 19(12):2000-4. DOI:10.3748/wjg.v19.i12.2000 · 2.37 Impact Factor
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