Effects of Mannitol and Dimethylthiourea on &lt;i&gt;Helicobacter pylori&lt;/i&gt;-Induced IL-8 Production in Gastric Epithelial Cells

Kim, Hye Young; Seo, Jae‐Hyun; Kim, Kyung Hwan

doi:10.1159/000028321

Cited by 40 publications

(47 citation statements)

References 25 publications

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“…3 However, our previous study showed that H. pylori-induced oxygen radicals in gastric epithelial cells in the absence of inflammatory cells. 4,5 These results demonstrate the possibility that H. pylori directly turns on transcription levels of inflammatory genes in gastric epithelial cells prior to the recruitment of inflammatory cells.…”

mentioning

confidence: 87%

“…A ratio of bacterium/cell was adapted from previous studies. 4,5,48 Supernatants were collected for the determination of IL-8 and MCP-1 at the indicated time points. The cells were homogenized and RNA was extracted for the determination of IL-8 and MCP-1 mRNA expression.…”

Section: Cell Line and H Pylori Infectionmentioning

confidence: 99%

“…HP99 was previously identified as cagA þ , vacA þ positive strain. 4,5 VacA, encoding the vacuolating toxin, is present in all strains, 45,54 and comprises two regions of allelic variation. 44 The s-region, located at the 5 0 end of the gene, and the m-region, located in the middle of vacA.…”

Section: Virulence Factors In H Pylori (Hp99)mentioning

confidence: 99%

“…15 Previously, we found that H. pylori increased lipid peroxidation, an indication of oxidative damage, and induced the activation of two species of NF-kB dimers (a p50/p65 heterodimer and a p50 homodimer) in gastric epithelial cells. 4,5 Pyrrolidine dithiocarbamate (PDTC), a proven free radical scavenger and NF-kB inhibitor, potentially inhibits NF-kB interaction with its upstream regulatory binding site thereby preventing NF-kBmediated transcriptional activation in H. pyloriinfected gastric epithelial cells. 16 22 Therefore, chemokine gene transcription may require the activation of the combination of NF-kB and AP-1, or that of NF-kB and CCAAT/enhancer binding protein (C/EBP).…”

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confidence: 99%

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Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

et al. 2003

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Oxidant-sensitive transcription factors, nuclear factor-jB (NF-jB), and activator protein-1 (AP-1) have been considered as the regulators of inducible genes such as chemokines. Since oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis, chemokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) may be regulated by NF-jB and/or AP-1. Ras, the upstream activator for mitogen-activated protein kinase (MAPK) and MAPK cascade regulate AP-1 activation. The present study aims to investigate whether H. pylori in a Korean isolate (HP99) induces the expression of chemokines (IL-8, MCP-1), which is regulated by Ras, MAPK, AP-1, and NF-jB in gastric epithelial AGS cells, and whether these transcriptional regulations of chemokines are inhibited by transfection with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IjBa (MAD-3) or treatment with MAPK inhibitors (U0126 for extracellular signal-regulated kinase or SB203580 for p38 kinase). In addition, virulence factors of HP99 were characterized by PCR analysis for the isolated DNA. As a result, HP99 is identified as cagA þ , vacA s1b, m2, iceA1 H. pylori strain. HP99 induced a time-dependent expression of mRNA and protein for IL-8 and MCP-1 via mediation of MAPK, AP-1, and NF-jB. Transfection with mutant genes for Ras, c-Jun, and IjBa and treatment with MAPK inhibitors suppressed H. pylori-induced activation of transcription factors (NF-jB, AP-1) and expression of chemokines (IL-8, MCP-1) in AGS cells. In conclusion, Ras and MAPK cascade may act as the upstream signaling for the activation of AP-1 and NF-jB, which induce chemokine expression in H. pylori-infected AGS cells. Specific targeting of the activation of NF-jB and AP-1 may be effective for the prevention or treatment of gastric inflammation associated with H. pylori infection.

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mentioning

confidence: 87%

Section: Cell Line and H Pylori Infectionmentioning

confidence: 99%

Section: Virulence Factors In H Pylori (Hp99)mentioning

confidence: 99%

mentioning

confidence: 99%

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Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

et al. 2003

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“…Interleukin-8 (IL-8), a member of the C-X-C chemokine family, is a potent chemoattractant and activator of neutrophils, monocytes, and T lymphocytes (3)(4)(5). ROS mediate the expression of IL-8 by activating oxidant-sensitive transcription factors in gastric epithelial cells (6)(7)(8).…”

mentioning

confidence: 99%

β-Carotene and Lutein Inhibit Hydrogen Peroxide-Induced Activation of NF-κB and IL-8 Expression in Gastric Epithelial AGS Cells

Kim

Seo

Kim

2011

J Nutr Sci Vitaminol

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Summary Reactive oxygen species (ROS) including hydrogen peroxide (H 2 O 2 ) are involved in the pathogenesis of gastric inflammation. Interleukin-8 (IL-8) is a potent mediator of the inflammatory response by activating and recruiting neutrophils to the site of infection. Oxidant-sensitive transcription factor NF-B regulates the expression of IL-8 in the immune and inflammatory events. Carotenoids (carotenes and oxygenated carotenoids) show antioxidant and anti-inflammatory activities. Low intake of ␤ -carotene leads to high risk of gastric cancer. Oxygenated carotenoid lutein inhibited NF-B activation in experimental uveitis. The present study aims to investigate whether ␤ -carotene and lutein inhibit H 2 O 2 -induced activation of NF-B and expression of IL-8 in gastric epithelial AGS cells. The cells were treated with carotenoids 2 h prior to the treatment of H 2 O 2 . mRNA expression was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR analyses. IL-8 level in the medium was determined by enzyme-linked immunosorbent assay. NF-B activation was assessed by electrophoretic mobility shift assay. ROS levels of the cells were detected by confocal microscopic analysis for fluorescent dichlorofluorescein. As a result, H 2 O 2 induced the activation of NF-B and expression of IL-8 in AGS cells time-dependently. ␤ -Carotene and lutein showed inhibitory effects on H 2 O 2 -induced increase in intracellular ROS levels, activation of NF-B, and IL-8 expression in AGS cells. In conclusion, supplementation of carotenoids such as ␤ -carotene and lutein may be beneficial for the treatment of oxidative stress-mediated gastric inflammation.

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Up regulation of GW112 Gene by NFκB promotes an antiapoptotic property in gastric cancer cells

Kim

Park

Song

et al. 2009

Molecular Carcinogenesis

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To clarify the regulatory mechanism of GW112 gene expression, 5'-flanking region of the human GW112 gene was isolated and characterized in the present study. 5'-RACE analysis showed a single transcription start site, which is located 142 nucleotides upstream of the translation initiation site. Transient transfection studies with serial deletion constructs and close examination of the sequences identified a putative NF kappaB binding sequence between -442 and -430, which could be responsible for efficient expression of the GW112 gene. Indeed, GW112 gene was found to be regulated by NF kappaB signals including overexpressed p65 and I kappaB alpha, IKK inhibitor, and proteasome inhibitor. Binding of NF kappaB to its putative site was confirmed by EMSA and ChIP assays. These results suggest that NF kappaB is an essential regulatory factor for GW112 transcription. Based on this finding, we next confirmed that inhibition of GW112 expression could induce apoptosis in the presence of cytotoxic agent in gastric cancer cells. Furthermore, knocking-down or overexpression of GW112 gene in gastric cancer cells demonstrated that GW112 has an antiapoptotic property against the cytotoxic agents-induced apoptosis. Taken together, these results suggest that GW112 could be an important mediator in NF kappaB-dependent tumorigenesis of digestive tract tissues.

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Effects of Mannitol and Dimethylthiourea on <i>Helicobacter pylori</i>-Induced IL-8 Production in Gastric Epithelial Cells

Cited by 40 publications

References 25 publications

Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

β-Carotene and Lutein Inhibit Hydrogen Peroxide-Induced Activation of NF-κB and IL-8 Expression in Gastric Epithelial AGS Cells

Up regulation of GW112 Gene by NFκB promotes an antiapoptotic property in gastric cancer cells

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