Ecabet sodium inhibits<i>Helicobacter pylori</i>lipopolysaccharide-induced activation of NADPH oxidase 1 or apoptosis of guinea pig gastric mucosal cells

Kusumoto, Kenji; Kawahara, Tsukasa; Kuwano, Yuki; Teshima-Kondo, Shigetada; Morita, Kyoko; Kishi, Kazushi; Rokutan, Kazuhito

doi:10.1152/ajpgi.00274.2004

Cited by 24 publications

(12 citation statements)

References 48 publications

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“…Taken together, our finding that VvpE induces proinflammatory responses via an ANXA2-dependent mechanism provides information about the important mechanisms of pathogen-induced cell death during V. vulnificus infection. Increasing evidence has suggested that lipid rafts are clustered to form a redox signaling platform through gp91 phox (NOX2) coupling with cytosolic factors that include p47 phox (NCF1), p67 phox (NCF2), and small GTPase Rac1 (45)(46)(47), and that these processes subsequently produce superoxides and other ROS (45). Although in most cell types, mitochondrial ROS are thought to be the largest contributor to intracellular ROS production (48), our result showed that the sequestration of cholesterol by MbCD attenuates intracellular ROS production and Expression of Ki67 (green) in ileum and jejunum was examined by confocal microscopy.…”

Section: Discussionmentioning

confidence: 99%

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Lee

Jung

Song

et al. 2015

The Journal of Immunology

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An inflammatory response is a hallmark of necrosis evoked by bacterial pathogens. Vibrio vulnificus, VvpE, is an elastase that is responsible for tissue necrosis and inflammation; however, the molecular mechanism by which it regulates host cell death has not been characterized. In the present study, we investigate the cellular mechanism of VvpE with regard to host cell death and the inflammatory response of human intestinal epithelial (INT-407) cells. The recombinant protein (r)VvpE (50 pg/ml) caused cytotoxicity mainly via necrosis coupled with IL-1β production. The necrotic cell death induced by rVvpE is highly susceptible to the knockdown of annexin A (ANXA)2 and the sequestration of membrane cholesterol. We found that rVvpE induces the recruitment of NADPH oxidase 2 and neutrophil cytosolic factor 1 into membrane lipid rafts coupled with ANXA2 to facilitate the production of reactive oxygen species (ROS). The bacterial signaling of rVvpE through ROS production is uniquely mediated by the phosphorylation of redox-sensitive transcription factor NF-κB. The silencing of NF-κB inhibited IL-1β production during necrosis. rVvpE induced hypomethylation and region-specific transcriptional occupancy by NF-κB in the IL-1β promoter and has the ability to induce pyroptosis via NOD-, LRR-, and pyrin domain–containing 3 inflammasome. In a mouse model of V. vulnificus infection, the mutation of the vvpE gene from V. vulnificus negated the proinflammatory responses and maintained the physiological levels of the proliferation and migration of enterocytes. These results demonstrate that VvpE induces the hypomethylation of the IL-1β promoter and the transcriptional regulation of NF-κB through lipid raft–dependent ANXA2 recruitment and ROS signaling to promote IL-1β production in intestinal epithelial cells.

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Section: Discussionmentioning

confidence: 99%

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Lee

Jung

Song

et al. 2015

The Journal of Immunology

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“…However, using the mouse model, only TLR2 and TLR4 have been proven to be related to atherogenesis (26,27), although it is conceivable that the other types of TLRs should be related as well. Nox1 expression-mediated control of TLR has been demonstrated in colon cells, where LPS produced by Helicobacter pylori is TLR4-dependent in inducing Nox1 expression (28). The presently known Nox1-inducing factors are IFN-␥ and 1␣,25-dihydroxyvitamin D 3 from intestinal epithelium (29,30), and angiotensin II, PGF 2 ␣, and platelet-derived growth factor from VSMCs (31,32).…”

Section: Discussionmentioning

confidence: 99%

Calcium-Independent Phospholipase A2β-Akt Signaling Is Involved in Lipopolysaccharide-Induced NADPH Oxidase 1 Expression and Foam Cell Formation

Lee

Park²,

Park³

et al. 2009

The Journal of Immunology

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Foam cell formation is the most important process in atherosclerosis, and low density lipoprotein oxidation by reactive oxygen species (ROS) is the key step in the conversion of macrophages to foam cells. This study reveals the control mechanism of the gene for NADPH oxidase 1 (Nox1), which produces ROS in the formation of foam cells by stimulating TLR4. Treatment of macrophages by the TLR4 agonist LPS stimulated ROS production and ROS-mediated macrophage to foam cell conversion. This LPS-induced ROS production and foam cell formation could be abrogated by pretreatment of macrophages with N-acetyl cysteine or apocynin. LPS increased Nox1 promoter activity, and resultant expression of mRNA and protein. Small interfering RNA mediated inhibition of Nox1 expression decreased LPS-induced ROS production and foam cell formation. LPS-mediated Nox1 expression and the responses occurred in a calcium-independent phospholipase A2 (iPLA2)-dependent manner. The iPLA2β-specific inhibitor S-BEL or iPLA2β small interfering RNA attenuated LPS-induced Nox1 expression, ROS production, and foam cell formation. In addition, activation of iPLA2β by LPS caused Akt phosphorylation and was followed by increased Nox1 expression. These results suggest that the binding of LPS and TLR4 increases Nox1 expression through the iPLA2β-Akt signaling pathway, and control ROS production and foam cell formation.

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“…There is evidence of species-specific distribution of Nox1 as well. Rodent stomach expresses Nox1, which has been shown to be upregulated by Helicobacter pylori lipopolysaccharide (LPS) [82, 83]. However, the expression of Nox1 in human stomach has been questioned [48], though another Nox isoform could play a similar role in humans.…”

Section: Nox Proteins In Signal Transductionmentioning

confidence: 99%

Nox proteins in signal transduction

Brown

Griendling

2009

Free Radical Biology and Medicine

748

688

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The NADPH oxidase (Nox) family of superoxide (O2•−) and hydrogen peroxide (H2O2) producing proteins has emerged as an important source of reactive oxygen species (ROS) in signal transduction. ROS produced by Nox proteins Nox1-5 and Duox1/2 are now recognized to play essential roles in the physiology of the brain, the immune system, the vasculature, the digestive tract, and hormone synthesis. Nox-derived ROS have been implicated in regulation of cytoskeletal remodeling, gene expression, proliferation, differentiation, migration and cell death. These processes are tightly controlled and reversible. In this review, we will discuss recent literature on Nox protein tissue distribution, subcellular localization, activation and the resulting signal transduction mechanisms.

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Ecabet sodium inhibitsHelicobacter pylorilipopolysaccharide-induced activation of NADPH oxidase 1 or apoptosis of guinea pig gastric mucosal cells

Abstract: . Ecabet sodium inhibits Helicobacter pylori lipopolysaccharide-induced activation of NADPH oxidase 1 or apoptosis of guinea pig gastric mucosal cells.

Cited by 24 publications

References 48 publications

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Calcium-Independent Phospholipase A2β-Akt Signaling Is Involved in Lipopolysaccharide-Induced NADPH Oxidase 1 Expression and Foam Cell Formation

Nox proteins in signal transduction

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