Long-term effects of Helicobacter pylori eradication on gastric antral mucosa in duodenal ulcer patients

Zerbib, Frank; Lenk, Christian; Sawan, Bassem; Cayla, R.; Broutet, Nathalie; Carles, Besses; Mascarel, A. De; Mégraud, Françis; Lamouliatte, H

doi:10.1097/00042737-200012070-00001

Cited by 35 publications

(35 citation statements)

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“…IM is also present in the antrum with duodenal ulcer, which is associated with lower risk of gastric cancer. 6 Thus, the predictive value of IM as a marker for the risk of developing gastric cancer is very low.…”

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confidence: 99%

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

et al. 2007

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Intestinal metaplasia is a key event in multistep gastric carcinogenesis. CDX2, a master regulator of intestinal phenotype, was shown to play a tumor-suppressive role in colon cancer. However, it was reported to be expressed in nearly all gastric intestinal metaplasia and many gastric cancers. As CDX2 is differentially expressed in normal stomach and intestine, we sought to relate the CDX2 expression to gastrointestinal differentiation along gastric carcinogenesis. The expression of CDX2 protein in gastric intestinal metaplasia, dysplasia and cancer was examined and related to their gastrointestinal differentiation. CDX2 expression was significantly decreased in incomplete intestinal metaplasia, which expresses both gastric mucins (MUC5AC and MUC6) and intestinal mucin (MUC2), compared with complete intestinal metaplasia, which expresses intestinal mucin (MUC2) only. Although incomplete intestinal metaplasia morphologically resembles colon, its CDX2 expression was apparently lower than that in the normal colon. Moreover, CDX2 expression was progressively reduced in gastric dysplasia and cancer. The CDX2 expression in gastric cancer was also inversely correlated with the expression of gastric mucins. As incomplete intestinal metaplasia is associated with higher risk of gastric cancer, its lower CDX2 expression compared with that in complete intestinal metaplasia and normal colon epithelium resolved the current contradiction between the tumor-suppressive role of CDX2 in the colon and the high prevalence of CDX2 in intestinal metaplasia. Further decrease of CDX2 expression in gastric dysplasia and cancer suggests that CDX2 plays a similar anticarcinogenic role in intestinal metaplasia as it does in colon. Intestinal metaplasia or dysplasia with low expression of CDX2 may serve as predictive markers for gastric cancer.

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confidence: 99%

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

et al. 2007

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“…If not treated, it is a lifelong infection whose implication in extra-digestive disease is suggested although not proven. Data coming from follow-up studies show that, after H. pylori eradication, in a subset of patients, chronic gastritis persists for months or even years (19,39), without a satisfactory explanation for this phenomenon. On the other hand, some data suggest a positive association between H. pylori infection and the development of food allergy (8,16) and other allergic manifestations (31,35) in humans.…”

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confidence: 99%

GastricHelicobacterInfection Inhibits Development of Oral Tolerance to Food Antigens in Mice

et al. 2003

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The increase in the transcellular passage of intact antigens across the digestive epithelium infected with Helicobacter pylori may interfere with the regulation of mucosal immune responses. The aim of this work was to study the capacity of Helicobacter infection to inhibit the development of oral tolerance or to promote allergic sensitization and the capacity of a gastro-protective agent, rebamipide, to interfere with these processes in mice. Oral tolerance to ovalbumin (OVA) was studied in 48 C3H/He 4-week-old mice divided into four groups: (i) OVA-sensitized mice; (ii) OVA-"tolerized" mice (that is, mice that were rendered immunologically tolerant); (iii) H. felis-infected, OVA-tolerized mice; (iv) and H. felis-infected, OVA-tolerized, rebamipide-treated mice. Oral sensitization to hen egg lysozyme (HEL) was studied in 48 mice divided into four groups: (i) controls; (ii) HEL-sensitized mice; (iii) H. felis-infected, HEL-sensitized mice; and (iv) H. felis-infected, HEL-sensitized, rebamipide-treated mice. Specific anti-OVA or anti-HEL immunoglobulin E (IgE) and IgG1/IgG2a serum titers were measured by enzyme-linked immunosorbent assay. Additionally, the capacity of rebamipide to interfere with antigen presentation and T-cell activation in vitro, as well as absorption of rebamipide across the epithelial monolayer, was tested. H. felis infection led to the inhibition of oral tolerance to OVA, but rebamipide prevented this inhibitive effect of H. felis. H. felis infection did not enhance the sensitization to HEL, but rebamipide inhibited the development of this sensitization. Moreover, rebamipide inhibited in a dose-dependent manner antigen presentation and T-cell activation in vitro and was shown to be able to cross the epithelium at a concentration capable of inducing this inhibitory effect. We conclude that H. felis can inhibit the development of oral tolerance to OVA in mice and that this inhibition is prevented by rebamipide.

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“…Long-term observation will therefore be required in clinical studies to obtain results analogous to those of the present animal study, and to clarify the usefulness of H. pylori eradication will probably require longer follow-up than the maximum of around 7 years in the clinical studies so far reported. [5][6][7][8][9] In this study, 30% to 40% of the animals examined died within 8 months of completion of therapy. Although the exact cause of death was not clear, he short lifespan of Mongolian gerbils appears to have been a factor.…”

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confidence: 61%

“…4 Although many studies have shown that eradication of H. pylori leads to resolution of inflammatory changes and reduction of cellular proliferation in the gastric mucosa, there have been conflicting findings on the effects of H. pylori eradication on gastric atrophy, intestinal metaplasia, and other diseases. [5][6][7][8][9] We previously reported that long-term infection with H. pylori ATCC 43504 caused various gastric intestinal diseases in Mongolian gerbils, including chronic gastritis, gastric atrophy (pseudopyloric glands), gastric ulcers, intestinal metaplasia, gastric carcinoid, and gastric adenocarcinoma, [10][11] and the reproducibility of this model has been confirmed by many researchers. [12][13] The aim of the present study was to determine the consequences of H. pylori eradication on the course of chronic gastritis, gastric atrophy, gastric ulcer, intestinal metaplasia, and gastric carcinoid in an H. pylori-inoculated animal model.…”

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confidence: 64%

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Long-term effects of Helicobacter pylori eradication in Mongolian gerbils

Hirayama¹,

Takagi²,

Yokoyama³

et al. 2002

Journal of Gastroenterology

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Long-term effects of Helicobacter pylori eradication on gastric antral mucosa in duodenal ulcer patients

Cited by 35 publications

References 0 publications

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

GastricHelicobacterInfection Inhibits Development of Oral Tolerance to Food Antigens in Mice

Long-term effects of Helicobacter pylori eradication in Mongolian gerbils

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