scholarly journals Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1750 ◽  
Author(s):  
Hanbit Lee ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Helicobacter Pylori ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Ags Cells ◽  
Compound C ◽  
H Pylori ◽  
Induced Apoptosis

Helicobacter pylori (H. pylori) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. AST inhibited H. pylori-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in H. pylori-stimulated cells. The number of LC3B puncta in H. pylori-stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

scholarly journals Vacuolating Cytotoxin of Helicobacter pylori Induces Apoptosis in the Human Gastric Epithelial Cell Line AGS

2001 ◽  
Vol 69 (8) ◽  
pp. 5080-5087 ◽  
Author(s):  
Dirk Kuck ◽  
Bernhard Kolmerer ◽  
Christof Iking-Konert ◽  
Peter H. Krammer ◽  
Wolfgang Stremmel ◽  
...  
Keyword(s):  
Cell Death ◽  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Potential Candidate ◽  
Ags Cells ◽  
Vacuolating Cytotoxin ◽  
Apoptosis Inducing Factor

ABSTRACT Helicobacter pylori induces cell death by apoptosis. However, the apoptosis-inducing factor is still unknown. The virulence factor vacuolating cytotoxin A (VacA) is a potential candidate, and thus its role in apoptosis induction was investigated in the human gastric epithelial cell line AGS. The supernatant from thevacA wild-type strain P12 was able to induce apoptotic cell death, whereas the supernatant from its isogenic mutant strain P14 could not. That VacA was indeed the apoptosis-inducing factor was demonstrated further by substantial reduction of apoptosis upon treatment of AGS cells with a supernatant specifically depleted of native VacA. Furthermore, a recombinant VacA produced inEscherichia coli was also able to induce apoptosis in AGS cells but failed to induce cellular vacuolation. These findings demonstrate that the vacuolating cytototoxin of H. pyloriis a bacterial factor capable of inducing apoptosis in gastric epithelial cells.

scholarly journals Effect of Di(2-ethylhexyl)phthalate onHelicobacter pylori-Induced Apoptosis in AGS Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Chuang-Hao Lin ◽  
Chien-Yi Wu ◽  
Hwang-Shang Kou ◽  
Chiao-Yun Chen ◽  
Meng-Chuan Huang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Food Packaging ◽  
Human Life ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Peptic Ulcers ◽  
Ags Cells ◽  
H Pylori ◽  
Ethylhexyl Phthalate

Plastic products are wildly used in human life. Di(2-ethylhexyl)phthalate (DEHP) is an essential additive in plastic manufacturing and is used as plasticizer for many products including plastic food packaging. DEHP is a teratogenic compound and can cause potent reproductive toxicity. DEHP can also cause liver damage, peroxisome proliferation, and carcinogenesis. DEHP is also strongly associated with peptic ulcers and gastric cancer; however, the underlying effect and mechanism of DEHP on the gastrointestinal tract are not entirely clear. The oral infection route ofH. pyloriparallels the major ingestion route of DEHP into the human body. Therefore, we wanted to study the effect of DEHP andH. pyloriexposure on the human gastric epithelial cell line, AGS (gastric adenocarcinoma). The viability of the AGS cell line was significantly lower in 80 μM-DEHP andH. pylori(MOI = 100 : 1) coexposure than DEHP orH. pylorialone. DEHP andH. pyloricoexposure also induced caspase-3 activation, and increased Bax/Bcl-2 ratio and DNA fragmentation in AGS cells. These results indicate that DEHP can enhanceH. pyloricytotoxicity and induce gastric epithelial cell apoptosis. Therefore, it is possible that DEHP andH. pyloricoexposure might enhance the disruption of the gastric mucosa integrity and potentially promote the pathogenesis of gastric carcinogenesis.

The effect of vacA allelic variation on the H. pylori-induced apoptosis in gastric epithelial cell line

2000 ◽  
Vol 118 (4) ◽  
pp. A1265
Author(s):  
Jongmin Lee ◽  
Yongchan Lee ◽  
Kwanghyoung Lee ◽  
Byounghyun Choe ◽  
Chaeyoon Chon ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Allelic Variation ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
H Pylori ◽  
Induced Apoptosis

scholarly journals Effect of Inhibition of Extracellular Signal-Regulated Kinase 1 and 2 Pathway on Apoptosis and bcl-2 Expression in Helicobacter pylori-Infected AGS Cells

2003 ◽  
Vol 71 (2) ◽  
pp. 830-837 ◽  
Author(s):  
Il Ju Choi ◽  
Joo Sung Kim ◽  
Jung Mogg Kim ◽  
Hyun Chae Jung ◽  
In Sung Song
Keyword(s):  
Gene Expression ◽  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Ags Cells ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Epithelial Cell Apoptosis ◽  
H Pylori ◽  
Induced Apoptosis

ABSTRACT Helicobacter pylori induces activation of mitogen-activated protein kinases (MAPKs). However, its effect on H. pylori-induced apoptosis has not been evaluated. Thus, we examined whether H. pylori-induced extracellular signal-regulated kinase 1 and 2 (ERK1/2) and p38 MAPK activation affects gastric epithelial cell apoptosis and bcl-2 family gene expression, especially in relation to the cagA status of an H. pylori strain. In flow cytometric and oligonucleosome-bound DNA enzyme-linked immunosorbent assay analyses, infection with cagA + H. pylori strains induced gastric cancer cell apoptosis in AGS cells more prominently than infection with cagA mutants. Activation of ERK1/2 and p38 MAPKs was also more prominent in cagA + strains. Pretreatment with a MEK inhibitor (PD98059) inhibited ERK1/2 activation and increased H. pylori-induced apoptosis significantly. This increased apoptosis was accompanied by decreased antiapoptotic bcl-2 mRNA expression among bcl-2-related genes (bcl-2, bax, bak, mcl-1, and bcl-XL/S ), and the effect was also more prominent in the cagA + strains. However, the alteration of bcl-2 gene expression was not accompanied by protein level changes. Inhibition of p38 using specific inhibitor SB203580 decreased H. pylori-induced apoptosis but resulted in little alteration of bcl-2-related gene expression. In conclusion, H. pylori-induced ERK1/2 activation, especially by the cagA + H. pylori strain, may play a protective role against gastric epithelial cell apoptosis partially through maintenance of bcl-2 gene expression.

scholarly journals Helicobacter pylori Activates Toll-Like Receptor 4 Expression in Gastrointestinal Epithelial Cells

2003 ◽  
Vol 71 (6) ◽  
pp. 3496-3502 ◽  
Author(s):  
Bin Su ◽  
Peter J. M. Ceponis ◽  
Sylvie Lebel ◽  
Hien Huynh ◽  
Philip M. Sherman
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Host Cells ◽  
Epithelial Cell Line ◽  
Type I ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
Tlr4 Mrna ◽  
H Pylori

ABSTRACT Helicobacter pylori activates the transcription factor NF-κB, leading to proinflammatory cytokine production by gastric epithelial cells. However, the receptors for the initial bacterial interaction with host cells which activate downstream signaling events have not been completely defined. Recently, it has been shown that microbial components activate Toll-like receptors (TLRs), thereby leading to AP-1- and NF-κB-dependent transcription and resulting in the production of proinflammatory cytokines. The aim of this study was to determine whether H. pylori activates TLR4. Reverse transcription-PCR showed that both type I and type II H. pylori clinical isolates induced TLR4 mRNA expression in AGS cells compared with that by uninfected controls. H. pylori upregulated TLR4 protein expression in two gastric epithelial cell lines (AGS and MKN45) and one intestinal epithelial cell line (T84). Monoclonal TLR4 antibody inhibited lipopolysaccharide-induced interleukin-8 secretion from THP-1 macrophages but not from gastric epithelial cells infected with H. pylori. H. pylori demonstrated increased adherence to CHO TLR4-transfected cells compared with that to both CHO TLR2-transfected and nontransfected CHO cells (P < 0.01). These results indicate that H. pylori activates TLR4 expression in epithelial cells and that TLR4 can serve as a receptor for H. pylori binding.

scholarly journals Rapid Interaction of Helicobacter pylori with Microvilli of the Polar Human Gastric Epithelial Cell Line NCI‐N87

2013 ◽  
Vol 296 (12) ◽  
pp. 1800-1805 ◽  
Author(s):  
Anne‐Kathrin Diesing ◽  
Constanze Nossol ◽  
Heidi Faber‐Zuschratter ◽  
Werner Zuschratter ◽  
Lydia Renner ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line
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