Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection

Ozawa, Kyoko; Kato, Seiichi; Sekine, Hitoshi; Koike, Tomoyuki; Minoura, Takanori; Iinuma, Kazuie; Nishimura, Hiroshi

doi:10.1007/s00535-004-1530-7

Cited by 19 publications

(22 citation statements)

References 40 publications

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“…Jones et al (33) showed that increased apoptosis and proliferation of gastric antral epithelial cells were observed in H. pylori-infected children, suggesting that the increased risk of gastric cancer development is associated with childhood acquisition of infection. In addition, our recent study demonstrated that epithelial cell apoptosis and proliferation are increased in the corpus as well as in the antrum in Japanese children with H. pylori infection, compared to those without infection (34). This altered epithelial cell turnover was improved after eradication of H. pylori (33,34).…”

Section: Discussionmentioning

confidence: 93%

“…In addition, our recent study demonstrated that epithelial cell apoptosis and proliferation are increased in the corpus as well as in the antrum in Japanese children with H. pylori infection, compared to those without infection (34). This altered epithelial cell turnover was improved after eradication of H. pylori (33,34). Prospective, long-term follow-up studies of Japanese children infected with H. pylori would help to answer the question about mild (grade 1) gastric atrophy based on the Sydney Classification system.…”

Section: Discussionmentioning

confidence: 96%

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Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

et al. 2006

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The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1-16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 96%

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

et al. 2006

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“…7). These changes are surprising because active chronic gastritis and associated oxidative stress induced by H. pylori are always more pronounced in the antral than in the corpus mucosa (6,15,40), which would predict a more severe injury of antral mitochondria. Yet this apparent controversy can be explained by a tissue type-specific control of the cellular bioenergetic processes by this bacterium.…”

Section: Different Oxidative Phosphorylation In the Corpus And Antralmentioning

confidence: 91%

Oxidative phosphorylation and its coupling to mitochondrial creatine and adenylate kinases in human gastric mucosa

Gruno

Peet²,

Seppet³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Energy metabolism in gastrobiopsy specimens of the antral and corpus mucosa, treated with saponin to permeabilize the cells, was studied in patients with gastric diseases. The results show twice lower oxidative capacity in the antral mucosa than in the corpus mucosa and the relative deficiency of antral mitochondria in complex I. The mucosal cells expressed mitochondrial and cytosolic isoforms of creatine kinase and adenylate kinase (AK). Creatine (20 mM) and AMP (2 mM) markedly stimulated mitochondrial respiration in the presence of submaximal ADP or ATP concentrations, and creatine reduced apparent Km for ADP in stimulation of respiration, which indicates the functional coupling of mitochondrial kinases to oxidative phosphorylation. Addition of exogenous cytochrome c increased ADP-dependent respiration, and the large-scale cytochrome c effect (>or=20%) was associated with suppressed stimulation of respiration by creatine and AMP in the mucosal preparations. These results point to the impaired mitochondrial outer membrane, probably attributed to the pathogenic effects of Helicobacter pylori. Compared with the corpus mucosa, the antral mucosa exhibited greater sensitivity to such type of injury as the prevalence of the large-scale cytochrome c effect was twice higher among the latter specimens. Active chronic gastritis was associated with decreased respiratory capacity of the corpus mucosa but with its increase in the antral mucosa. In conclusion, human gastric mucosal cells express the mitochondrial and cytosolic isoforms of CK and AK participating in intracellular energy transfer systems. Gastric mucosa disease is associated with the altered functions of these systems and oxidative phosphorylation.

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“…45,46 Because some cytokines released from infl ammatory cells are known to have an inhibitory effect on gastric acid secretion, 47,48 such residual lymphocyte infi ltration may be partly responsible for the regional functional irreversibility. Many investigations have demonstrated that H. pylori infection alters the kinetic pattern of the gastric glandular epithelium, resulting in an increase in epithelial proliferation, [22][23][24][25][26][27] and that pathological changes induced by the infection such as infl ammatory infi ltration 34,35,49 or mucosal atrophy concomitant with intestinal metaplasia [24][25][26][27] are each related to the gastric epithelial hyperproliferation. However, some controversy exists concerning the effects of its eradication on the epithelial hyperproliferation.…”

Section: Ki-67 Labeling Indexmentioning

confidence: 99%

Sustained epithelial proliferation in a functionally irreversible fundic mucosa after Helicobacter pylori eradication

et al. 2009

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Functionally irreversible (non-acid-secreting) gastric mucosa after eradication was associated with extensive intestinal metaplasia and sustained hyperproliferation, suggesting that such mucosa still possesses malignant potential. Congo red chromoendoscopy may be useful for estimating the risk of subsequent development of gastric cancer following successful H. pylori eradication by determining the distribution of functionally irreversible mucosa.

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Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection

Abstract: H. pylori infection induced gastric mucosal inflammation and epithelial cell turnover in children. Moreover, gastric mucosal defense mechanism against H. pylori infection was activated. H. pylori eradication in childhood might prevent the accumulation of gastric epithelial cell damage.

Cited by 19 publications

References 40 publications

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

Association Between Gastric Atrophy and Helicobacter pylori Infection in Japanese Children: A Retrospective Multicenter Study

Oxidative phosphorylation and its coupling to mitochondrial creatine and adenylate kinases in human gastric mucosa

Sustained epithelial proliferation in a functionally irreversible fundic mucosa after Helicobacter pylori eradication

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