scholarly journals Effects ofHelicobacter pyloriand Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Liping Tao ◽  
Hai Zou ◽  
Zhimin Huang
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Mtt Assay ◽  
Heat Shock Protein 70 ◽  
Hsp70 Expression ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
H Pylori

Infection ofHelicobacter pylori (H. pylori)changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects ofH. pylorion the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further investigation.Objective.To investigate the effects ofHelicobacter pylori (H. pylori)and heat shock protein 70 (HSP70) on the proliferation of human gastric epithelial cells.Methods. H. pyloriand a human gastric epithelial cell line (AGS) were cocultured. The proliferation of AGS cells was quantitated by an MTT assay, and the expression of HSP70 in AGS cells was detected by Western blotting. HSP70 expression in AGS cells was silenced by small interfering RNA (siRNA) to investigate the role of HSP70. ThesiRNA-treated AGS cells were cocultured withH. pyloriand cell proliferation was measured by an MTT assay.Results.The proliferation of AGS cells was accelerated by coculturing withH. pylorifor 4 and 8 h, but was suppressed at 24 and 48 h. HSP70 expression was decreased in AGS cells infected byH. pylorifor 48 h. The proliferation in HSP70-silenced AGS cells was inhibited after coculturing withH. pylorifor 24 and 48 h compared with the control group.Conclusions.Coculture ofH. pylorialtered the proliferation of gastric epithelial cells and decreased HSP70 expression. HSP70 knockdown supplemented the inhibitory effect ofH. pylorion proliferation of epithelial cells. These results indicate that the effects ofH. pylorion the proliferation of gastric epithelial cells at least partially depend on the decreased expression of HSP70 induced by the bacterium.

The effect of the heat shock protein 70 on Helicobacter-pylori infected gastric epithelial cells

1998 ◽  
Vol 114 ◽  
pp. A239
Author(s):  
N. Nakajima ◽  
H. Kuwayama ◽  
Y. Ito ◽  
S. Hayakawa ◽  
A. Iwasaki ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Gastric Epithelial Cells

scholarly journals Helicobacter pylori Induces Gastric Epithelial Cell Apoptosis in Association with Increased Fas Receptor Expression

1999 ◽  
Vol 67 (8) ◽  
pp. 4237-4242 ◽  
Author(s):  
Nicola L. Jones ◽  
Andrew S. Day ◽  
Hilary A. Jennings ◽  
Philip M. Sherman
Keyword(s):  
Cell Death ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Receptor Expression ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
Fas Receptor ◽  
Epithelial Cell Apoptosis ◽  
H Pylori

ABSTRACT The mechanisms involved in mediating the enhanced gastric epithelial cell apoptosis observed during infection withHelicobacter pylori in vivo are unknown. To determine whether H. pylori directly induces apoptosis of gastric epithelial cells in vitro and to define the role of the Fas-Fas ligand signal transduction cascade, human gastric epithelial cells were infected with H. pylori for up to 72 h under microaerophilic conditions. As assessed by both transmission electron microscopy and fluorescence microscopy, incubation with acagA-positive, cagE-positive, VacA-positive clinical H. pylori isolate stimulated an increase in apoptosis compared to the apoptosis of untreated AGS cells (16.0% ± 2.8% versus 5.9% ± 1.4%, P < 0.05) after 72 h. In contrast, apoptosis was not detected following infection withcagA-negative, cagE-negative, VacA-negative clinical isolates or a Campylobacter jejuni strain. In addition to stimulating apoptosis, infection with H. pylorienhanced Fas receptor expression in AGS cells to a degree comparable to that of treatment with a positive control, gamma interferon (12.5 ng/ml) (148% ± 24% and 167% ± 24% of control, respectively). The enhanced Fas receptor expression was associated with increased sensitivity to Fas-mediated cell death. Ligation of the Fas receptor with an agonistic monoclonal antibody resulted in an increase in apoptosis compared to the apoptosis of cells infected with the bacterium alone (38.5% ± 7.1% versus 16.0% ± 2.8%,P < 0.05). Incubation with neutralizing anti-Fas antibody did not prevent apoptosis of H. pylori-infected cells. Taken together, these findings demonstrate that the gastric pathogen H. pylori stimulates apoptosis of gastric epithelial cells in vitro in association with the enhanced expression of the Fas receptor. These data indicate a role for Fas-mediated signaling in the programmed cell death that occurs in response toH. pylori infection.

Lactobacillus fermentum UCO-979C beneficially modulates the innate immune response triggered by Helicobacter pylori infection in vitro

2018 ◽  
Vol 9 (5) ◽  
pp. 829-841 ◽  
Author(s):  
V. Garcia-Castillo ◽  
H. Zelaya ◽  
A. Ilabaca ◽  
M. Espinoza-Monje ◽  
R. Komatsu ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Morphological Changes ◽  
Helicobacter Pylori Infection ◽  
Lactobacillus Fermentum ◽  
Gastric Tissue ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
H Pylori

Helicobacter pylori infection is associated with important gastric pathologies. An aggressive proinflammatory immune response is generated in the gastric tissue infected with H. pylori, resulting in gastritis and a series of morphological changes that increase the susceptibility to cancer development. Probiotics could present an alternative solution to prevent or decrease H. pylori infection. Among them, the use of immunomodulatory lactic acid bacteria represents a promising option to reduce the severity of chronic inflammatory-mediated tissue damage and to improve protective immunity against H. pylori. We previously isolated Lactobacillus fermentum UCO-979C from human gastric tissue and demonstrated its capacity to reduce adhesion of H. pylori to human gastric epithelial cells (AGS cells). In this work, the ability of L. fermentum UCO-979C to modulate immune response in AGS cells and PMA phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 (human monocytic leukaemia) macrophages in response to H. pylori infection was evaluated. We demonstrated that the UCO-979C strain is able to differentially modulate the cytokine response of gastric epithelial cells and macrophages after H. pylori infection. Of note, L. fermentum UCO-979C was able to significantly reduce the production of inflammatory cytokines and chemokines in AGS and THP-1 cells as well as increase the levels of immunoregulatory cytokines, indicating a remarkable anti-inflammatory effect. These findings strongly support the probiotic potential of L. fermentum UCO-979C and provide evidence of its beneficial effects against the inflammatory damage induced by H. pylori infection. Although our findings should be proven in appropriate experiments in vivo, in both H. pylori infection animal models and human trials, the results of the present work provide a scientific rationale for the use of L. fermentum UCO-979C to prevent or reduce H. pylori-induced gastric inflammation in humans.

scholarly journals Inhibitory Effect of β-Carotene on Helicobacter pylori-Induced TRAF Expression and Hyper-Proliferation in Gastric Epithelial Cells

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 637 ◽  
Author(s):  
Yongchae Park ◽  
Hanbit Lee ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Gastric Epithelial Cells ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
H Pylori ◽  
Β Carotene

Helicobacter pylori infection causes the hyper-proliferation of gastric epithelial cells that leads to the development of gastric cancer. Overexpression of tumor necrosis factor receptor associated factor (TRAF) is shown in gastric cancer cells. The dietary antioxidant β-carotene has been shown to counter hyper-proliferation in H. pylori-infected gastric epithelial cells. The present study was carried out to examine the β-carotene mechanism of action. We first showed that H. pylori infection decreases cellular IκBα levels while increasing cell viability, NADPH oxidase activity, reactive oxygen species production, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, and TRAF1 and TRAF2 gene expression, as well as protein–protein interaction in gastric epithelial AGS cells. We then demonstrated that pretreatment of cells with β-carotene significantly attenuates these effects. Our findings support the proposal that β-carotene has anti-cancer activity by reducing NADPH oxidase-mediated production of ROS, NF-κB activation and NF-κB-regulated TRAF1 and TRAF2 gene expression, and hyper-proliferation in AGS cells. We suggest that the consumption of β-carotene-enriched foods could decrease the incidence of H. pylori-associated gastric disorders.

scholarly journals α-Lipoic Acid Inhibits IL-8 Expression by Activating Nrf2 Signaling in Helicobacter pylori-infected Gastric Epithelial Cells

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2524 ◽  
Author(s):  
Seoyeon Kyung ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Oxidative Stress ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Lipoic Acid ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Gastric Epithelial Cells ◽  
Gastric Diseases ◽  
Ags Cells ◽  
H Pylori

Helicobacter pylori (H. pylori) causes gastritis and gastric cancers. Oxidative stress is involved in the pathological mechanism of H. pylori-induced gastritis and gastric cancer induction. Therefore, reducing oxidative stress may be beneficial for preventing the development of H. pylori-associated gastric diseases. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a crucial regulator for the expression of antioxidant enzyme heme oxygenase-1 (HO-1), which protects cells from oxidative injury. α-Lipoic acid (α-LA), a naturally occurring dithiol, shows antioxidant and anti-inflammatory effects in various cells. In the present study, we examined the mechanism by which α-LA activates the Nrf2/HO-1 pathway, suppresses the production of pro-inflammatory cytokine interleukine-8 (IL-8), and reduces reactive oxygen species (ROS) in H. pylori-infected AGS cells. α-LA increased the level of phosphorylated and nuclear-translocated Nrf2 by decreasing the amount of Nrf2 sequestered in the cytoplasm by complex formation with Kelch-like ECH1-associated protein 1 (KEAP 1). By using exogenous inhibitors targeting Nrf2 and HO-1, we showed that up-regulation of activated Nrf2 and of HO-1 results in the α-LA-induced suppression of interleukin 8 (IL-8) and ROS. Consumption of α-LA-rich foods may prevent the development of H. pylori-associated gastric diseases by decreasing ROS-mediated IL-8 expression in gastric epithelial cells.

scholarly journals Ceramide and Toll-Like Receptor 4 Are Mobilized into Membrane Rafts in Response to Helicobacter pylori Infection in Gastric Epithelial Cells

2012 ◽  
Vol 80 (5) ◽  
pp. 1823-1833 ◽  
Author(s):  
Dah-Yuu Lu ◽  
Hui-Chen Chen ◽  
Mei-Shiang Yang ◽  
Yuan-Man Hsu ◽  
Hwai-Jeng Lin ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Lipid Rafts ◽  
Gastric Epithelial Cells ◽  
Toll Like Receptor ◽  
Tlr4 Expression ◽  
Ags Cells ◽  
Content Type ◽  
Infected Cells ◽  
H Pylori

ABSTRACTHelicobacter pyloriinfection is thought to be involved in the development of several gastric diseases. TwoH. pylorivirulence factors (vacuolating cytotoxin A and cytotoxin-associated gene A) reportedly interact with lipid rafts in gastric epithelial cells. The role of Toll-like receptor (TLR)-mediated signaling in response toH. pyloriinfection has been investigated extensively in host cells. However, the receptor molecules in lipid rafts that are involved inH. pylori-induced innate sensing have not been well characterized. This study investigated whether lipid rafts play a role inH. pylori-induced ceramide secretion and TLR4 expression and thereby contribute to inflammation in gastric epithelial cells. We observed that both TLR4 and MD-2 mRNA and protein levels were significantly higher inH. pylori-infected AGS cells than in mock-infected cells. Moreover, significantly more TLR4 protein was detected in detergent-resistant membranes extracted fromH. pylori-infected AGS cells than in those extracted from mock-infected cells. However, this effect was attenuated by the treatment of cells with cholesterol-usurping agents, suggesting thatH. pylori-induced TLR4 signaling is dependent on cholesterol-rich microdomains. Similarly, the level of cellular ceramide was elevated and ceramide was translocated into lipid rafts afterH. pyloriinfection, leading to interleukin-8 (IL-8) production. Using the sphingomyelinase inhibitor imipramine, we observed thatH. pylori-induced TLR4 expression was ceramide dependent. These results indicate the mobilization of ceramide and TLR4 into lipid rafts byH. pyloriinfection in response to inflammation in gastric epithelial cells.

scholarly journals Induction of secretion of interleukin-8 from human gastric epithelial cells by heat-shock protein 60 homologue of Helicobacter pylori

1999 ◽  
Vol 48 (10) ◽  
pp. 927-933 ◽  
Author(s):  
Hiroyuki Yamaguchi ◽  
Takako Osaki ◽  
Naoto Kurihara ◽  
Masaki Kitajima ◽  
Masanori Kai ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Interleukin 8 ◽  
Heat Shock Protein 60 ◽  
Gastric Epithelial Cells

scholarly journals Inhibitory Effect of Astaxanthin on Helicobacter pylori- Induced Matrixmetalloproteinase Expression in Gastric Epithelial AGS Cells

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1132-1132
Author(s):  
Jimin Lee ◽  
Suji Bae ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Oxidative Stress ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Cell Invasion ◽  
Pcr Analysis ◽  
Epithelial Cell Line ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
Extracellular Matrix Components ◽  
H Pylori

Abstract Objectives Matrix metalloproteinases (MMPs), enzymes capable of degrading extracellular matrix components (ECM), are believed to be associated with carcinogenesis. Helicobacter pylori (H. pylori) infection increased oxidative stress and promotes the invasion and metastasis of gastric cells by inducing expression of MMPs. Reactive oxygen species (ROS) mediates expression of MMPs. Astaxanthin, a xanthophyll carotenoid, has strong antioxidant and anticancer properties. The present study was aimed to investigate whether astaxanthin inhibits H. pylori-induced MMPs expression in human gastric epithelial cells by redicing oxidative stress. Methods AGS cells, human gastric epithelial cell line, were pre-treated with astaxanthin for 3 hours prior to H. pylori (cag A positive NCTC 11,637 strains) infection. The cells treated with or without astaxanthin were cultured for 24 hours in the presence of H. pylori. mRNA expression of MMP-7 and MMP-10 was measured by real time PCR analysis. ROS levels were determined using dichlorofluorescin fluorescence. Protein levels of MMPs were determined using western blot analysis. Invasion assay was performed for the cells in the upper and lower compartments in Matrigel-coated filters and the cells were examined under a laser scanning confocal microscope. Results H. pylori increased ROS levels and expression of MMP-7 and MMP-10 in AGS cells. H. pylori induced cell invasion. Astaxanthin suppressed the expression of H. pylori-induced MMP-7 and MMP-10 at the mRNA and protein level. Conclusions H. pylori infection induces expression of MMP-7 and MMP-10 and cell invasion, which may be mediated with increased ROS in gastric epithelial cells. Astaxanthin inhibits MMP expression by reducingROS levels in H. pylori-infected gastric epithelial cells. Funding Sources This study was supported by a Brain Korea 21 FOUR Project, Yonsei University, Seoul, Republic of Korea.

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