Helicobacter Pylori Pathogenicity
Mostrando 13-24 de 92 artigos, teses e dissertações.
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13. The effect of CagA status on response to Helicobacter pylori eradication therapy in Western Turkey
If cytotoxin-associated gene A (CagA) status affects the response rates of therapy, then it may be possible to predict Helicobacter pylori eradication rates. We aimed to evaluate the response to eradication treatment of H. pylori infection in CagA-positive and CagA-negative patients. A total of 184 patients (93 males, 91 females, mean age 42.6 ± 12.8 years)
Brazilian Journal of Medical and Biological Research. Publicado em: 2001-11
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14. Proteins Encoded by the cag Pathogenicity Island of Helicobacter pylori Are Required for NF-κB Activation
Helicobacter pylori is the etiological agent in the development of chronic gastritis, duodenal ulceration, and gastric adenocarcinoma. The difference in virulence between individual strains is reflected in their ability to induce interleukin-8 (IL-8) secretion from gastric epithelial cells. It has been shown that virulence is associated with the presence of
American Society for Microbiology.
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15. Helicobacter pylori cag Pathogenicity Island Is Associated with Reduced Expression of Interleukin-4 (IL-4) mRNA and Modulation of the IL-4δ2 mRNA Isoform in Human Gastric Mucosa
Interleukin-4 (IL-4) and IL-4δ2 mRNA gastric expression was evaluated in healthy subjects and patients who did not have ulcers but were infected with Helicobacter pylori with or without the cag pathogenicity island (cag PAI). IL-4 mRNA was physiologically expressed by gastric epithelium and negatively influenced by H. pylori. Also, nonepithelial cells in th
American Society for Microbiology.
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16. Pathogenicity of Helicobacter pylori: a perspective.
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17. Helicobacter pylori CagA activates NF-κB by targeting TAK1 for TRAF6-mediated Lys 63 ubiquitination
Helicobacter pylori-initiated chronic gastritis is characterized by the cag pathogenicity island-dependent upregulation of proinflammatory cytokines, which is largely mediated by the transcription factor nuclear factor (NF)-κB. However, the cag pathogenicity island-encoded proteins and cellular signalling molecules that are involved in H. pylori-induced NF-
Nature Publishing Group.
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18. Helicobacter pylori Induces AGS Cell Motility and Elongation via Independent Signaling Pathways
Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosp
American Society for Microbiology.
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19. Characterization and Immunogenicity of the CagF Protein of the cag Pathogenicity Island of Helicobacter pylori
Helicobacter pylori infection causes severe gastroduodenal diseases in humans. Its virulence is strongly increased by the presence of the cag pathogenicity island (cag PAI). It has been shown that CagA, a major antigen in humans, is translocated to the host cell via a secretion system encoded by the cag PAI. The roles of many of the proteins encoded within t
American Society for Microbiology.
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20. Helicobacter pylori Induces Apoptosis of Human Monocytes but Not Monocyte-Derived Dendritic Cells: Role of the cag Pathogenicity Island†
Monocytes are circulating precursors of the dendritic cell subset, professional antigen-presenting cells with a unique ability to initiate the innate and adaptive immune response. In this study, we have investigated the effects of wild-type Helicobacter pylori strains and their isogenic mutants with mutations in known bacterial virulence factors on monocytes
American Society for Microbiology.
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21. A whole-genome microarray reveals genetic diversity among Helicobacter pylori strains
Helicobacter pylori colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the gen
The National Academy of Sciences.
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22. Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses
Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori–colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to path
American Society for Clinical Investigation.
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23. Determination of Helicobacter pylori Virulence by Simple Gene Analysis of the cag Pathogenicity Island
Nucleic acid amplification was performed for five loci in the cag pathogenicity island (PAI) of Helicobacter pylori (comprising cagA, the cagA promoter region, cagE, cagT, and the left end of cagII [LEC]), and gastric inflammation in patients was evaluated. Of 204 H. pylori isolates from Japanese patients (53 with peptic ulcer, 55 with gastric cancer, and 96
American Society for Microbiology.
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24. Helicobacter pylori Infection Induces Interleukin-8 Receptor Expression in the Human Gastric Epithelium
The gastric pathogen Helicobacter pylori is known to activate multiple proinflammatory signaling pathways in epithelial cells. In this study, we addressed the question of whether expression of the interleukin-8 receptors IL-8RA (CXCR1) and IL-8RB (CXCR2) is upregulated in H. pylori-infected human gastric biopsy samples. Biopsy samples from patients infected
American Society for Microbiology.