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Sugiyama, Atsushi; Ikeno, Tatsuo; Ishida, Kumiko; Maruta, Fukuto; Murakami, Maki; Sato, Toshiyuki; Saito, Hiroyasu; Ishizone, Satoshi; Kawasaki, Seiji; Ota, Hiroyoshi; Katsuyama, Tsutomu

doi:10.1023/a:1012367602010

Cited by 7 publications

(3 citation statements)

References 19 publications

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Section: Discussionsupporting

confidence: 92%

“…This is in keeping with the observation by Sugiyama et al [40], who demonstrated that ethanol damage was greatly limited in the HP -infected stomach of Mongolian gerbils. These investigators concluded that HP infection exhibits a paradoxical influence on mucosal defense by enhancing the resistance of the gastric mucosa to damage induced by necrotizing irritants [40]. This ‘protective’ action of an HP infection was not fully clarified in Sugiyama et al’s [40]study, but increased generation of PGE 2 derived from COX-2 expression due to HP infection was proposed to explain the beneficial effect of an HP infection against the injurious effect of a topical irritant such as alcohol.…”

Section: Discussionsupporting

confidence: 92%

“…These investigators concluded that HP infection exhibits a paradoxical influence on mucosal defense by enhancing the resistance of the gastric mucosa to damage induced by necrotizing irritants [40]. This ‘protective’ action of an HP infection was not fully clarified in Sugiyama et al’s [40]study, but increased generation of PGE 2 derived from COX-2 expression due to HP infection was proposed to explain the beneficial effect of an HP infection against the injurious effect of a topical irritant such as alcohol. We have confirmed this in the present study using repetitive treatment with HP LPS.…”

Section: Discussionmentioning

confidence: 99%

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Enhanced Resistance of Gastric Mucosa to Damaging Agents in the Rat Stomach Adapted to <i>Helicobacter pylori</i> Lipopolysaccharide

Brzozowski

Konturek²,

Moran³

et al. 2003

Digestion

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Background and Aim: Lipopolysaccharide (LPS) has been proposed to act as one of numerous virulence factors in the Helicobacter pylori (HP)-infected stomach. However, little is known as to whether the gastric mucosa can withstand the repeated LPS insult, and how the possible adaptation to this endotoxin influences the damage induced by strong irritants. We determined the effect of a single or repeated parenteral administration of LPS obtained from HP on acute gastric lesions induced by intragastric application of 100% ethanol (1.5 ml) and by water immersion and restraint stress (WRS). Methods: The area of the gastric lesions was measured by planimetry, mucosal gastric blood flow (GBF) was determined by H₂ gas clearance, and gastric luminal content was collected for the determination of luminal NO₂^–/NO₃^– levels by the Griess reaction. Biopsy samples were taken for the measurement of prostaglandin (PG) E₂ by radioimmunoassay and mucosal expression of constitutive and inducible nitric oxide synthase (cNOS and iNOS), constitutive (COX-1) and inducible cyclooxygenase (COX-2), heat shock protein 70 (HSP 70) mRNA and protein were analyzed by RT-PCR and Western blot. Results:HP LPS (1 mg/kg i.p.) injected once or 5 times produced negligible macroscopic injury and failed to influence GBF significantly compared to the injuries recorded in vehicle-controlled rats. Single and repeated (5 times) administration of HP LPS significantly reduced ethanol- and WRS-induced lesions, these protective effects were accompanied by a rise in GBF and excessive luminal release of NO. The suppression of NOS activity by L-NAME (20 mg/kg i.p.), a nonspecific NOS inhibitor, or L- (30 mg/kg i.g.), a specific iNOS inhibitor, and of COX-2 activity by NS-398 reversed the protective and hyperemic effects of single or repeated LPS administrations against ethanol and WRS damage and the accompanying rise in NO and PGE₂ production. These effects of L-NAME were significantly antagonized by the addition of L-arginine, a substrate for NO synthesis. The signals for cNOS, COX-1 and HSP 70 mRNA were detected by RT-PCR in the vehicle-treated gastric mucosa, whereas gene and protein expression of iNOS, COX-2 and HSP 70 mRNA were significantly increased only in rats treated with 1 or 5 applications of HP LPS. Conclusions: Repeated injections of HP LPS enhance gastric mucosal resistance to the mucosal damage induced by ethanol and WRS via a mechanism involving mucosal overexpression of iNOS, COX-2 and HSP 70 with subsequent excessive production of NO and PGE₂.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Enhanced Resistance of Gastric Mucosa to Damaging Agents in the Rat Stomach Adapted to <i>Helicobacter pylori</i> Lipopolysaccharide

Brzozowski

Konturek²,

Moran³

et al. 2003

Digestion

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Suppressive effect of rice extract on Helicobacter pylori infection in a Mongolian gerbil model

et al. 2005

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The Association Between cagA+ H. pylori Infection and Distal Gastric Cancer: A Proposed Model

2004

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Cytotoxin-associated gene A (cagA)+ infection is associated with an increased risk of distal gastric cancer. The aim was to determine the effect of Helicobacter pylori (HP) on gastric mucus thickness, hydrophobicity, and PGE2 and their relation to colonization density. Ninety-nine patients were recruited (69 HP- and 30 HP+: 10 cagA+, 18 cagA-, 2 undetermined) and six biopsies were obtained from each patient. Mucus thickness, hydrophobicity, PGE2, and colonization density were determined. HP status was assessed by histology and culture; cagA+ was determined by PCR. In age- and sex-matched patients, PGE2 was greater in PH+ than HP- (P = 0.04), with cagA+ having higher PGE2 than HP- patients (P = 0.031). No differences were observed in mucus thickness (P = 0.717) or hydrophobicity (P = 0.27) between HP+ and HP- patients. However, cagA+ showed a nonsignificant trend of increase in mucus thickness (P = 0.784) and hydrophobicity (P = 0.30) compared to cagA- and HP- patients. cagA+ colonization density was weakly correlated with increased thickness (r = 0.333, P = 0.381), whereas cagA- density was inversely correlated with thickness (r = -0.805, P = 0.0001). A model suggesting the possible changes induced by cagA+ infection is proposed which explains the high association of cagA+ with distal gastric cancer. If supported by large multicenter studies, this could form the basis for the development of new therapies directed at the mucous layer to eradicate HP and thus reduce the risk of gastric cancer.

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Cited by 7 publications

References 19 publications

Enhanced Resistance of Gastric Mucosa to Damaging Agents in the Rat Stomach Adapted to <i>Helicobacter pylori</i> Lipopolysaccharide

Enhanced Resistance of Gastric Mucosa to Damaging Agents in the Rat Stomach Adapted to <i>Helicobacter pylori</i> Lipopolysaccharide

Suppressive effect of rice extract on Helicobacter pylori infection in a Mongolian gerbil model

The Association Between cagA+ H. pylori Infection and Distal Gastric Cancer: A Proposed Model

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