Helicobacter pylori-induced Expression of Interleukin-8 and Cyclooxygenase-2 in AGS Gastric Epithelial Cells: Mediation by Nuclear Factor-κB

Kim, H.; Lim, Joo Weon; Kim, K. H.

doi:10.1080/003655201300191969

Cited by 66 publications

(43 citation statements)

References 53 publications

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“…The adhesion of H. pylori to gastric epithelial cells was reported to activate nuclear factor kappa B (NFκB) and stimulate IL-8 production. 37) Yamaoka et al reported a remarkable increase of IL-6 and IL-8 levels in GC tissues, and concluded that IL-8 levels in GC tissues are largely independent of H. pylori infection. 38) In conclusion, the IL-8 level measured in drainage veins may reflect IL-8 production mainly by the primary lesion, and is valuable as an prognostic indicator or a risk factor for recurrence in GC patients, whereas the peripheral level of IL-8 is not.…”

Section: Discussionmentioning

confidence: 99%

The role of circulating IL‐8 and VEGF protein in the progression of gastric cancer

et al. 2003

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Both vascular endothelial growth factor (VEGF) and interleukin 8 (IL-8) play an important role in the progression of gastric cancer (GC). In this study, we investigated whether circulating levels of VEGF or IL-8 in drainage veins of GC patients were correlated with any clinicopathological factors. Thirty-seven patients with primary GC who underwent gastrectomy at our department between 1999 and 2002 were analyzed. Blood samples were drawn from a peripheral vein just before surgery and from a drainage vein immediately after laparotomy. Plasma VEGF levels were significantly higher than those in 10 healthy controls. There was no correlation between VEGF levels in drainage veins and any clinicopathological variable, whereas there was a significant relationship in the case of VEGF levels in peripheral veins; the levels were higher in patients with venous invasion. We found a significant relationship between IL-8 levels in drainage veins and both tumor size and lymph node metastasis, whereas no significant relationship between IL-8 levels in peripheral veins and any variable was found. There was no correlation between VEGF and IL-8 levels in drainage veins. Large tumors, deeply invasive tumors, lymph node involvement, venous invasion and high IL-8 levels in drainage veins were all significantly associated with shorter diseasefree survival, although multivariate analysis revealed that lymph node involvement was the only independent prognostic factor. In conclusion, the measurement of IL-8 levels in drainage veins of GC patients may reflect production mainly by the primary lesion and is valuable as an indicator of risk for recurrent disease.

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Section: Discussionmentioning

confidence: 99%

The role of circulating IL‐8 and VEGF protein in the progression of gastric cancer

et al. 2003

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“…The activation of NF-B with bacterial products (such as P. aeruginosa LPS) may trigger a proinflammatory and hyperproliferative cellular phenotype that, when deranged, can lead to neoplasia (such as cholesteatoma) or even contribute downstream gene products to the chronic inflammatory milieus that leads to malignancy (47). H. pylori infection induces cell proliferation (48) and overexpression of IL-8 and cyclooxygenase-2 in gastric epithelial cells (49), both events that may play a causative role in gastric carcinoma. Similarly, NF-B-mediated proinflammatory dysregulation has been associated with both the development of pancreatic cancer (50) and the progression to metastases (51).…”

Section: Discussionmentioning

confidence: 99%

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Preciado

Caicedo

Jhanjee

et al. 2005

The Journal of Immunology

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NF-κB is activated during acute inflammatory states as well as in other injury response disease states. Several pathologic states in squamous tissue injury response are characterized by increased squamous proliferation. This study was performed to investigate the hypothesis that Pseudomonas aeruginosa LPS is able to activate a proliferative phenotype in squamous cells via NF-κB induction and that this NF-κB-mediated response may be abrogated with the classic anti-inflammatory agent indomethacin. EMSA, luciferase reporter gene experiments, Western blots, and cellular proliferation assays were performed in normal and transformed human keratinocytes after stimulation with P. aeruginosa LPS. EMSA and luciferase reporter gene assays showed a 3- to 5-fold induction of active NF-κB in human keratinocyte cell lines after stimulation with P. aeruginosa LPS. The stimulation correlated with significantly increased cellular proliferation. As one potential mechanism for this increase in proliferation, an NF-κB-specific activation of cyclin D1 was observed. Both the NF-κB induction and proliferation response were inhibited with indomethacin and in dominant negative stable transfection clones. P. aeruginosa LPS activates proliferation of human keratinocytes, potentially through the induction of NF-κB and cyclin D1. These findings suggest that bacterial components can contribute to proliferative disease states in squamous epithelium through NF-κB activation.

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“…pylori Infection of AGS Cells-The AGS human gastric epithelial cell line (gastric adenocarcinoma, ATCC CRL 1739) was obtained from the American Type Culture Collection (Manassas, VA). The cells were grown in RPMI 1640 medium (Invitrogen) supplemented with 10% fetal bovine serum (Invitrogen) in the presence of 100 units/ml penicillin-streptomycin at 37°C in a humidified chamber in 5% CO 2 (18). The cells were seeded at 1 ϫ 10 6 cells/dish in 10-cm cell culture dishes, grown to 80% confluency, and then washed twice with PBS, pH 7.4, and the medium was replaced with antibiotic-free RPMI 1640 medium.…”

Section: Methodsmentioning

confidence: 99%

Subcellular and Functional Proteomic Analysis of the Cellular Responses Induced by Helicobacter pylori

Chan

Chang

et al. 2006

Molecular & Cellular Proteomics

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Helicobacter pylori infection is a crucial factor in the pathogenesis of several digestive disorders, including peptic ulcers, chronic gastritis, and gastric cancer. Moreover H. pylori induces disease-specific protein expression in gastric epithelial cells. The aim of the present study was to characterize proteins differentially expressed in H. pylori-infected gastric epithelial AGS cells. An in vitro model was established using a multiplicity of infection of 100 and evaluating the effectiveness of H. pylori infection by functional analyses. Changes in protein patterns were identified using a proteomic approach consisting of two-dimensional fluorescence difference gel electrophoresis and mass spectrometry. The expression of many proteins was found to be altered, and 28 of these were identified and classified as protein synthesis-and folding-related proteins, cytoskeleton proteins, metabolic enzymes, transcription-and translation-related proteins, angiogenesis/ metastasis-related proteins, cell communication/signal transduction-related proteins, or others (oxygen-regulated protein and oncoprotein). The expression profiles of eight of these proteins, laminin ␥-1 chain precursor, valosin-containing protein, heat shock 70-kDa protein, mitochondrial matrix protein P1, FK506-binding protein 4, Tcomplex protein 1, enolase ␣, and 14-3-3 ␤ were further examined in cancerous and paired surrounding normal tissues by immunoblot assay and immunohistochemical staining to identify molecular targets that may be involved in the pathogenesis of H. pylori-induced gastric diseases. On the basis of our results, valosin-containing protein, mitochondrial matrix protein P1, T-complex protein 1, enolase ␣, and 14-3-3

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Helicobacter pylori-induced Expression of Interleukin-8 and Cyclooxygenase-2 in AGS Gastric Epithelial Cells: Mediation by Nuclear Factor-κB

Abstract: NF-kappaB may play a novel role in expression of IL-8 and COX-2 in H. pylori-induced gastric inflammation.

Cited by 66 publications

References 53 publications

The role of circulating IL‐8 and VEGF protein in the progression of gastric cancer

The role of circulating IL‐8 and VEGF protein in the progression of gastric cancer

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Subcellular and Functional Proteomic Analysis of the Cellular Responses Induced by Helicobacter pylori

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