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  • 1
    Electronic Resource
    Electronic Resource
    Up-Regulation of Inducible Nitric Oxide Synthase and Nitric Oxide in Helicobacter pylori-Infected Human Gastric Epithelial Cells: Possible Role of Interferon-γ in Polarized Nitric Oxide Secretion (2002)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 7 (2002), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Nitric oxide (NO) generated by nitric oxide synthase (NOS) is known to be an important modulator of the mucosal inflammatory response. In this study, we questioned whether Helicobacter pylori infection could up-regulate the epithelial cell inducible NOS (iNOS) gene expression and whether NO production could show polarity that can be regulated by immune mediators.Materials and Methods. Human gastric epithelial cell lines were infected with H. pylori, and the iNOS mRNA expression was assessed by quantitative RT-PCR. NO production was assayed by determining nitrite/nitrate levels in culture supernatants. To determine the polarity of NO secretion by the H. pylori-infected epithelial cells, Caco-2 cells were cultured as polarized monolayers in transwell chambers, and NO production was measured.Results. iNOS mRNA levels were significantly up-regulated in the cells infected with H. pylori, and expression of iNOS protein was confirmed by Western blot analysis. Increased NO production in the gastric epithelial cells was seen as early as 18 hours postinfection, and reached maximal levels by 24 hours postinfection. The specific MAP kinase inhibitors decreased H. pylori-induced iNOS and NO up-regulation. After H. pylori infection of polarized epithelial cells, NO was released predominantly into the apical compartment, and IL-8 was released predominantly into basolateral compartment. The addition of IFN-γ to H. pylori-infected polarized epithelial cells showed a synergistically higher apical and basolateral NO release.Conclusion. These results suggest that apical NO production mediated by MAP kinase in H. pylori-infected gastric epithelial cells may influence the bacteria and basolateral production of NO and IL-8 may play a role in the tissue inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1083-4389.2002.00068.x
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  • 2
    Electronic Resource
    Electronic Resource
    Caspase-3 Activity and Expression of Bcl-2 Family in Human Neutrophils by Helicobacter pylori Water-Soluble Proteins (2001)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 6 (2001), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Persistent infiltration of neutrophils is an almost invariable feature of Helicobacter pylori-infected gastric mucosa. A prolongation of neutrophil life-span could contribute to the pathogenesis of H. pylori infection. Recently, we have demonstrated that H. pylori water extracts (HPWE) inhibited neutrophil apoptosis. To elucidate the regulation of intracellular apoptotic signals by HPWE, we examined the activity of caspase-8, -3 and expression of Bcl-2 family in neutrophils.〈section xml:id="abs1-3"〉〈title type="main"〉Materials and methods.Human neutrophils were obtained from the peripheral blood of healthy volunteers by density gradient separation. HPWE was prepared from a supernatant of the H. pylori suspension in distilled water. After neutrophils were incubated with HPWE, expression of Bcl-2 family [antiapoptotic (Bcl-2, Bcl-XL and Mcl-1) and proapoptotic (Bax, Bak and Bcl-XS)] was determined by RT-PCR and Western blotting, respectively. Western blot for Bcl-2 family also performed in neutrophilic differentiated HL-60 cells by all-trans-retinoic acid. The activity of caspase-8, -3 was measured by the detection of p-nitroanilide after cleavage from labeled substrate.〈section xml:id="abs1-4"〉〈title type="main"〉Results.HPWE suppressed the activation of caspase-8 and -3, and upregulated the expression of Bcl-XL mRNA and proteins in neutrophils. The expression of Bax and Bak was upregulated and Bcl-2, Bcl-XL and Mcl-1 downregulated in HL-60 cells during neutrophilic differentiation.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion.Bcl-XL may have an important role in the neutrophilic development and inhibition of neutrophil apoptosis by H. pylori.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2001.00030.x
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of Helicobacter pylori-induced Nuclear Factor-kappa B Activation and Interleukin-8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells (2003)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 8 (2003), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Helicobacter pylori stimulates nuclear factor-kappa B (NF-κB) activation and chemokine interleukin-8 (IL-8) expression in gastric epithelial cells. Ecabet sodium (ecabet), a locally acting antiulcer drug, is known to have anti-H. pylori activity. However, there is little understanding of how ecabet induces anti-inflammatory activity in gastric epithelial cells infected with H. pylori. The aim of this study was to investigate the effects of ecabet on IL-8 gene expression and NF-κB activation in human gastric epithelial cells infected with H. pylori.Materials and Methods.  After Hs746T, MKN-45, or SNU-5 gastric epithelial cell lines had been infected with cagA+cytotoxin+H. pylori in the presence of ecabet, IL-8 mRNA expression was assessed by quantitative reverse transcription–polymerase chain reaction, and IL-8 secretion was measured by enzyme-linked immunosorbent assay. NF-κB and inhibitory kappa B-alpha (IκBα) signals were assayed by electrophoretic mobility shift assay and Western blot, respectively. The activation of NF-κB and IL-8 reporter genes was determined by luciferase assay.Results.  Ecabet showed no antimicrobial activiy against Gram-positive or -negative bacteria. However, ecabet inhibited transcription of the IL-8 gene and secretion of IL-8 by gastric epithelial cells infected with H. pylori at a concentration of 5 µg/ml. Moreover, ecabet inhibited the activation of NF-κB and the degradation of IκBα in gastric epithelial cells in response to H. pylori infection. In addition, the NF-κB signal inhibited by ecabet was comprised predominantly of heterodimers of p65/p50.Conclusions.  Ecabet inhibited H. pylori-induced IL-8 gene transcription and secretion by suppressing the NF-κB signal. This inhibition might be one pathway by which ecabet exerts its anti-inflammatory effect on H. pylori-induced gastric inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1523-5378.2003.00175.x
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition of Proinflammatory Cytokine Expression by NF-κB (p65) Antisense Oligonucleotide in Helicobacter pylori-Infected Mice (2005)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 10 (2005), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-κB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-κB in vivo. The aim of this study was to evaluate the role of nuclear factor-κB on the expressions of proinflammatory cytokines in H. pylori-infected mice.Materials and Methods.  We evaluated nuclear factor-κB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-κB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-κB (p65).Results.  In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-κB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-α and interleukin-1β concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-κB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-κB and the expressions of tumor necrosis factor-α and interleukin-1β in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines.Conclusions.  H. pylori infection was found to activate the expressions of proinflammatory cytokines via nuclear factor-κB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1523-5378.2005.00365.x
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  • 5
    Electronic Resource
    Electronic Resource
    Virulence factors of Helicobacter pylori in Korean isolates do not influence proinflammatory cytokine gene expression and apoptosis in human gastric epithelial cells, nor do these factors influence the clinical outcome (2000)
    Springer
    Journal of gastroenterology 35 (2000), S. 898-906 
    Details
    ISSN: 1435-5922
    Keywords: Key words: apoptosis ; cytokine ; gastric epithelial cells ; Helicobacter pylori ; virulence factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: The cytotoxin-associated gene (cagA) and vacuolating cytotoxin (Vac) production have been reported to be major virulence factors of Helicobacter pylori. However, there have been some disputes regarding the correlation between these virulence factors and clinical outcomes. We evaluated whether the cagA-positive genotype and Vac production might be cor-related with various gastroduodenal diseases in Korea and whether this correlation could be due to differences in proinflammatory cytokine gene expression and apoptosis of gastric epithelial cells in vitro. The presence of the cagA gene was examined by the polymerase chain reaction (PCR), and Vac production was detected using the bacterial culture supernatant and HeLa cells after H. pylori was isolated from Korean patients. Gastric epithelial cells were infected with cagA +Vac+, cagA +Vac−, or cagA −Vac− strains, after which cytokine gene expression was evaluated, using quantitative reverse transcription (RT)-PCR. Apoptosis and caspase-3 activation were measured in H. pylori-infected gastric epithelial cells. There was no significant correlation between the presence of these virulence factors in H. pylori isolates and peptic ulcer or gastric cancer. Upregulation of cytokine gene expression, including that of interleukin (IL)-1α, IL-8, granulocyte macrophage colony-stimulating factor (GM-CSF), and monocyte chemotactic protein (MCP)-1, as well as apoptosis and caspase-3 activation, were similar in infections with cagA-positive and cagA-negative strains, but were not correlated with the production of Vac. These results suggest that the lack of correlation between virulence factors of isolated H. pylori strains and serious gastroduodenal disease entities in Korea may be due to the similar capacity for proinflammatory cytokine gene expression and apoptosis caused by infection with each of the H. pylori strains.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005350070003
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  • 6
    Electronic Resource
    Electronic Resource
    Upregulated Cyclooxygenase-2 Inhibits Apoptosis of Human Gastric Epithelial Cells Infected with Helicobacter pylori (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 2436-2443 
    Details
    ISSN: 1573-2568
    Keywords: apoptosis ; cyclooxygenase-2 ; gastric epithelial cells ; Helicobacter pylori ; prostaglandin E2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Helicobacter pylori induces apoptosis and alters the proliferation of gastric mucosal epithelial cells. Cyclooxygenase-2 (COX-2), the inducible form of prostaglandin (PG) synthesis, is known to cause alteration in epithelial cell growth. The goal of this study was to determine whether COX-2 gene expression by H. pylori infection could influence gastric epithelial cell apoptosis. Expression of COX-2 mRNA and proteins was up-regulated in Hs746T gastric epithelial cell lines infected with H. pylori, when assessed by quantitative RT-PCR and western blot. Inhibition of COX-2 expression using NS-398, a specific COX-2 inhibitor, showed a significant increase of gastric epithelial cell apoptosis and caspase-3 activation in Hs746T cells infected with H. pylori. Moreover, the effect of NS-398 on H. pylori-induced apoptosis was reversed by the addition of PGE2. These results suggest that up-regulated COX-2 expression by H. pylori infection can inhibit apoptosis of gastric epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005611613542
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  • 7
    Electronic Resource
    Electronic Resource
    Helicobacter pylori Water-Soluble Surface Proteins Activate Human Neutrophils and Up-Regulate Expression of CXC Chemokines (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 83-92 
    Details
    ISSN: 1573-2568
    Keywords: Helicobacter pylori ; neutrophil ; chemokine ; quantitative RT-PCR ; calcium ; myeloperoxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the mechanisms of the persistent neutrophil recruitment in H. pylori-infected gastric mucosa, we evaluated the activation of human neutrophils and CXC chemokine expression in neutrophils by H. pylori water-soluble surface proteins. H. pylori water extract (HPWE) was prepared from a supernatant of the H. pylori suspension in distilled water. After neutrophils were stimulated with HPWE, the mobilization of intracellular free calcium, the expression of lymphocyte function-associated antigen-1β, and the secretion of myeloperoxidase (MPO) were enhanced in the neutrophils. In H. pylori-infected gastric mucosa, transendothelial and transepithelial migration of neutrophils were observed by electron microscopy and mucosal MPO levels were elevated. Up-regulation of the expression of interleukin-8 (IL-8) and growth-related oncogenes (GROs; GROα, GROβ and GROγ) mRNA and protein in neutrophils by HPWE was demonstrated by quantitative reverse transcription–polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. In conclusion, H. pylori-induced neutrophil recruitment may be mediated by CXC chemokines which are expressed by neutrophils activated by H. pylori water-soluble surface proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005461427250
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