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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
    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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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    Long-Term Effects of Helicobacter pylori Eradication on Intestinal Metaplasia in Patients with Duodenal and Benign Gastric Ulcers (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 1754-1762 
    Details
    ISSN: 1573-2568
    Keywords: Helicobacter pylori ; intestinal metaplasia ; eradication ; duodenal ulcer ; gastric ulcer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was conducted to investigate whether or not the eradication of H. pylori could lead to the regression of intestinal metaplasia (IM) in patients with either duodenal ulcer (DU) or benign gastric ulcer (BGU). The initial antral IM grade was 0.21 in the 72 patients of the H. pylori-eradicated DU group, this decreased to 0.17, 0.14, 0.13, and 0.09 after periods of four weeks, one year, two years, and four years, respectively, but without statistical significance. In the corpus of the DU group, where IM grade was low (0.02), there was no detectable change in IM. The initial antral IM grade of 0.69 in the 41 patients of the H. pylori-eradicated BGU group decreased substantially to 0.61, 0.44, and 0.39 after periods of four weeks and one and two years, respectively, but again without statistical significance. The initial corporal IM grade of the BGU group of 0.27 decreased to 0.20, 0.15, and 0.06 after periods of four weeks and one and two years, again without statistical significance. In contrast, the IM grades of the noneradicated DU group (N = 20) and the BGU group (N = 16) showed nearly no change in the antrum and corpus. Gastritis grades of antrum and corpus in the H. pylori-eradicated DU or BGU group significantly decreased with respect to time (P = 0.0001), but there were no significant changes in the corresponding noneradicated groups. Although there was no statistical significance, IM decreased in the antrum and corpus of the stomach with BGU and in antrum of those with DU over a two to four-year period after H. pylori eradication, suggesting the possible reversibility of IM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005534328511
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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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  • 8
    Electronic Resource
    Electronic Resource
    Long-term clinical course and prognostic factors in intestinal Behçet's Disease (2000)
    Springer
    Diseases of the colon & rectum 43 (2000), S. 692-700 
    Details
    ISSN: 1530-0358
    Keywords: Behçet's Disease ; Intestinal disease ; Reoperation ; Recurrence ; Azathioprine ; Intestinal perforation ; Hemicolectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract PURPOSE: The present study was aimed at evaluating the long-term course of intestinal Behçet's disease and determining predictive factors of prognosis. METHODS: This report is a retrospective study based on the records of 43 patients with intestinal Behçet's disease. The mean follow-up duration was 73±60 months. We evaluated the efficacy of medical treatment for the intestinal lesion at initial eight weeks. The cumulative probabilities were calculated by using Kaplan-Meier method, and the results were compared by using the log-rank test. RESULTS: Sixteen patients (38 percent) achieved a complete remission of intestinal lesions eight weeks after medical treatment had begun. The patients who achieved a complete remission had a lower probability of receiving an operation than those who had not (13 percent at 2 and 5 yearsvs. 36 and 43 percent, respectively;P=0.028). The recurrence probability of intestinal lesions was 25 percent at two years and 49 percent at five years after complete remission with medical treatment. Patients who had a history of intestinal perforation or fistula had a higher probability of recurrence after operation than those without such history (59vs. 33 percent at 2 years; 88vs. 57 percent at 5 years;P=0.020). Patients who had taken azathioprine had a lower probability of receiving reoperation than those who did not (7vs. 25 percent at 2 years; 25vs. 47 percent at 5 years;P=0.035). The length of ileal resection and whether hemicolectomy was performed had no significant effect on the recurrence or reoperation rate. CONCLUSIONS: Intestinal Behçet's disease frequently requires a surgical treatment and has a high recurrence rate. The patients who achieved a complete remission with medical treatment, who had no history of intestinal performation, and who received azathioprine after operation showed better clinical courses. Resection of a short segment of bowel would be a more appropriate surgical procedure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02235590
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