NSAIDs counteractH. pyloriVacA toxin-induced cell vacuolation in MKN 28 gastric mucosal cells

2002 ◽  
Vol 283 (3) ◽  
pp. G511-G520 ◽  
Author(s):  
Vittorio Ricci ◽  
Barbara A. Manzo ◽  
Concetta Tuccillo ◽  
Patrice Boquet ◽  
Ulderico Ventura ◽  
...  
Keyword(s):  
Cultured Cells ◽  
Mucosal Injury ◽  
Channel Activity ◽  
Cell Binding ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Chloride Channel Blocker ◽  
Inflammatory Drugs ◽  
H Pylori ◽  
The Relationship

The relationship between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori-induced gastric mucosal injury is still under debate. VacA toxin is an important H. pylori virulence factor that causes cytoplasmic vacuolation in cultured cells. Whether and how NSAIDs affect VacA-induced cytotoxicity is unclear. This study was designed to evaluate the effect of NSAIDs on H. pylori VacA toxin-induced cell vacuolation in human gastric mucosal cells in culture (MKN 28 cell line). Our data show that 1) NSAIDs (indomethacin, aspirin, and NS-398) inhibit VacA-induced cell vacuolation independently of inhibition of cell proliferation and prostaglandin synthesis; 2) NSAIDs impair vacuole development/maintenance without affecting cell binding and internalization of VacA; and 3) NSAIDs, as well as the chloride channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid, also inhibit cell vacuolation induced by ammonia. We thus hypothesize that NSAIDs might protect MKN 28 cells against VacA-induced cytotoxicity by inhibiting VacA channel activity required for vacuole genesis.

Induction of apoptotic DNA fragmentation by nonsteroidal anti-inflammatory drugs in cultured rat gastric mucosal cells

1998 ◽  
Vol 360 (2-3) ◽  
pp. 273-280 ◽  
Author(s):  
Hidenobu Kusuhara ◽  
Hirofumi Matsuyuki ◽  
Mamoru Matsuura ◽  
Tomonori Imayoshi ◽  
Takeki Okumoto ◽  
...  
Keyword(s):  
Dna Fragmentation ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

TNFα induced by H. Pylori phosphorylates JNK pathway which may induce apoptosis in gastric mucosal cells

1998 ◽  
Vol 114 ◽  
pp. A1168
Author(s):  
A. Nagahara ◽  
H. Miwa ◽  
M. Hirose ◽  
H. Misawa ◽  
M. Kawabe ◽  
...  
Keyword(s):  
Gastric Mucosal Cells ◽  
Jnk Pathway ◽  
Mucosal Cells ◽  
H Pylori

Release of somatostatinlike immunoreactivity from canine fundic mucosal cells in primary culture

1984 ◽  
Vol 247 (5) ◽  
pp. G558-G566 ◽  
Author(s):  
A. H. Soll ◽  
T. Yamada ◽  
J. Park ◽  
L. P. Thomas
Keyword(s):  
Cultured Cells ◽  
Time Dependent ◽  
Small Cells ◽  
Dependent Manner ◽  
Secretory Function ◽  
Dibutyryl Camp ◽  
Gastric Mucosal Cells ◽  
Steady Rate ◽  
Somatostatin Cells ◽  
Mucosal Cells

We have developed a model to allow study of the release of somatostatinlike immunoreactivity (SLI) from gastric mucosal cells. Collagenase-dispersed canine fundic mucosal cells were separated by counterflow elutriation. SLI-containing cells were identified in the fractions with small cells (9-11 microns), and these fractions were plated onto collagen. After 2 days in culture, SLI content of the cells was maintained; SLI-positive cells, detected by peroxidase-antiperoxidase immunohistochemistry, comprised 70 +/- 6% (mean +/- SE, n = 6) of these cultured cells. Release of SLI from these cultures into the medium was determined by radioimmunoassay. Epinephrine, dibutyryl cAMP, and gastrin each stimulated SLI release in a time-dependent manner, with a steady rate of secretion maintained for 120 min of incubation. Both epinephrine and dibutyryl cAMP markedly potentiated the release of SLI stimulated by gastrin but were not themselves mutually potentiating. Upon Sephadex G-50 column chromatography of incubation medium and extracts of cultured cells, SLI eluted primarily in a single peak that cochromatographed with synthetic somatostatin tetradecapeptide. Our data suggest that gastrin and adrenergic stimuli act directly on canine fundic somatostatin cells and that potentiating interactions between secretagogues may be important modulating elements in somatostatin cell secretory function.

Helicobacter pylorilipopolysaccharide induces apoptosis of cultured guinea pig gastric mucosal cells

2001 ◽  
Vol 281 (3) ◽  
pp. G726-G734 ◽  
Author(s):  
Tsukasa Kawahara ◽  
Shigetada Teshima ◽  
Yuki Kuwano ◽  
Ayuko Oka ◽  
Kyoichi Kishi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cytochrome C ◽  
Guinea Pig ◽  
Primary Cultures ◽  
Specific Inhibitor ◽  
Caspase 8 ◽  
Cytochrome C Release ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
H Pylori

Helicobacter pylori lipopolysaccharide (LPS) is generally accepted as a low-toxicity virulence. Primary cultures of guinea pig gastric mucosal cells expressed the Toll-like receptor 4 and were sensitive to H. pylori LPS as well as Escherichia coli LPS. H. pylori LPS stimulated phosphorylation of transforming growth factor-β-activated kinase 1 (TAK1), TAK1-binding protein 1 (TAB1), and c-Jun NH2-terminal kinase (JNK) 2. H. pylori LPS at >2.1 endotoxin unit/ml (>1 ng/ml) activated caspase-8, stimulated cytochrome c release from mitochondria, and subsequently activated caspases-9 and -3, leading to apoptosis. Epidermal growth factor blocked all of these apoptotic processes and inhibited apoptosis, whereas it did not modify the phosphorylation of TAK1, TAB1, and JNK2. A comparatively specific inhibitor of caspase-8 or -9 blocked apoptosis, whereas cytochrome c release was prevented only with a caspase-8-like inhibitor. Our results suggest that caspase-8 and mitochondria may play crucial roles in H. pylori LPS-induced apoptosis and that this accelerated apoptosis may be involved in abnormal cell turnover of H. pylori-infected gastric mucosa.

scholarly journals Heme Oxygenase-1 Protects Gastric Mucosal Cells against Non-steroidal Anti-inflammatory Drugs

2006 ◽  
Vol 281 (44) ◽  
pp. 33422-33432 ◽  
Author(s):  
Mayuko Aburaya ◽  
Ken-Ichiro Tanaka ◽  
Tatsuya Hoshino ◽  
Shinji Tsutsumi ◽  
Keitarou Suzuki ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

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

2005 ◽  
Vol 288 (2) ◽  
pp. G300-G307 ◽  
Author(s):  
Kenji Kusumoto ◽  
Tsukasa Kawahara ◽  
Yuki Kuwano ◽  
Shigetada Teshima-Kondo ◽  
Kyoko Morita ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Nadph Oxidase ◽  
Transforming Growth Factor ◽  
Polyacrylamide Gel Electrophoresis ◽  
Northern Hybridization ◽  
Gastric Mucosal Cells ◽  
Ecabet Sodium ◽  
Nadph Oxidase 1 ◽  
Mucosal Cells ◽  
H Pylori

Helicobacter pylori LPS activates a homolog of gp91phox, NADPH oxidase 1 (Nox1), in guinea pig gastric mucosal cells cultured in 10% FBS-containing medium. RT-PCR and Northern hybridization demonstrated that H. pylori LPS stimulated expression of Nox1 and a novel p47phoxhomolog (Noxo1) mRNAs with a peak at 4 h, followed by upregulation of superoxide anion (O2−) generation. Pretreatment with 10 mg/ml of a nonabsorbable antigastric ulcer drug, ecabet sodium (ecabet), completely blocked these two mRNA expressions and the upregulation of O2−production. Under low (0.1%)-FBS conditions, H. pylori LPS predominantly caused apoptosis of the cells. Ecabet completely blocked the LPS-triggered phosphorylation of transforming growth factor-β-activated kinase 1 (TAK1) and TAK1-binding protein 1, activation of caspase 8, loss of mitochondrial membrane potential, release of cytochrome c, activation of caspase 3, and appearance of apoptotic cells. In contrast, ecabet had no effect on ethanol- or etoposide-initiated apoptosis. The ecabet-pretreated cells exhibited the responsiveness to H. pylori LPS, similarly as untreated control cells did, when ecabet was removed by washing before the addition of H. pylori LPS. Incubation of H. pylori LPS with ecabet eliminated the toxic effects of the LPS, and nondenatured polyacrylamide gel electrophoresis indicated the formation of higher molecular mass complexes between H. pylori LPS and ecabet, suggesting that ecabet may interact with H. pylori LPS and block the activation of Toll-like receptor 4 (TLR4). Our results suggest that ecabet may suppress TLR4-mediated inflammation or accelerated apoptosis caused H. pylori infection.

scholarly journals L-GLUTAMINE ERADICATES HELICOBACTER PYLORI GASTRITIS: A NOVEL CASE REPORT

2017 ◽  
Vol 10 (10) ◽  
pp. 13
Author(s):  
Balaji Ommurugan ◽  
Amita Priya
Keyword(s):  
Helicobacter Pylori ◽  
Sports Medicine ◽  
Gastrointestinal Diseases ◽  
Epithelial Proliferation ◽  
Gastric Mucosal Cells ◽  
First Case ◽  
Mucosal Cells ◽  
H Pylori ◽  
Common Infection ◽  
Helicobacter Pylori Gastritis

  Helicobacter pylori is the most common infection causing gastrointestinal diseases in the developing countries. It causes oxidative damage to gastric mucosal cells thereby altering the epithelial proliferation of these cells. With proton pump inhibitors and antibiotics being the mainstay in the management of symptoms, preclinical and clinical research is making inroads with novel therapeutic innovations to target the bacterium with the help of antioxidants. Hence, we report the first case of the treatment and eradication of H. pylori using L-glutamine, a sports medicine supplement with high antioxidant potential.

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