Effect of Helicobacter pylori infection and eradication on gastric epithelial cell proliferation and apoptosis

Unger, Zsuzsa; Molnár, Béla; Szaleczky, Erika; Törgyekes, Edina; Müller, Ferenc; Zágoni, Tamás; Tulassay, Zsolt; Pajor, László

doi:10.1016/s0928-4257(01)00048-1

Cited by 14 publications

(12 citation statements)

References 21 publications

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“…In previous studies, patients with H. pylori infection and chronic gastritis exhibited significantly increased rates of epithelial cell proliferation. Cell proliferation decreases after successful H. pylori eradication [30, 31]. Although the mean Ki-67 index was decreased (decreased cell proliferation) following H. pylori eradication in our study, there was no significant difference in mean Ki-67 index between patients with IM and those without IM.…”

Section: Discussioncontrasting

confidence: 51%

“…Although the mean Ki-67 index was decreased (decreased cell proliferation) following H. pylori eradication in our study, there was no significant difference in mean Ki-67 index between patients with IM and those without IM. The condition of gastric mucosal cell proliferation might be due to the status of H. pylori infection and chronic gastritis, but not the status of IM [30, 31]. …”

Section: Discussionmentioning

confidence: 99%

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Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

et al. 2017

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BackgroundGastric epithelial hyper-proliferation was reported in patients with Helicobacter pylori (H. pylori)–infected gastric mucosa with intestinal metaplasia (IM) changes. In patients with gastric ulcer (GU) and IM, the GU may have a different healing rate in comparison to patients without IM. This study aimed to compare the difference in GU healing between H. pylori–infected patients with IM and those without IM.MethodsWe retrospectively analyzed patients at the Keelung Chung Gung Memorial Hospital during the period from March 2005 to January 2011. The inclusion criteria were: 1) endoscopic findings of GU and biopsy histological examination plus rapid urease test indicating H. pylori infection; 2) gastric IM adjacent to a GU but with no atrophic gastritis changes; 3) patients receiving H. pylori eradication triple therapy and 8 weeks of maintenance therapy with a proton pump inhibitor; and 4) patients receiving follow-up endoscopy within the 3rd and the 4th months after treatment.ResultsIn total, 327 patients with GU and H. pylori infection (136 with IM and 191 without IM) were included. Patients with IM had a higher GU healing rate than those without IM (91.9% vs. 84.3%, P = 0.040). Multivariate logistical regression analysis revealed that failure of H. pylori eradication (Odds = 4.013, 95% CI: 1.840–8.951, P < 0.001) and gastric IM (Odds = 0.369, 95% CI: 0.168–0.812, P = 0.013) were the predictors of non-healing GU following treatment.ConclusionsPatient with gastric IM change may have a higher GU healing rate than those without gastric IM. However, successful H. pylori eradication is a more important factor for GU healing than gastric IM.

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Section: Discussioncontrasting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

et al. 2017

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“…20,21 Apoptosis associated with H. pylori is also associated with increased epithelial proliferation, whereas, in areas of IM or dysplasia, proliferation remains increased but apoptosis reverts to normal levels following H. pylori eradication. 5,[22][23][24][25] Gastric IM is categorized into three types: I (complete), and II and III (incomplete). Type III IM typically shows the greatest genetic changes.…”

Section: Discussionmentioning

confidence: 99%

Epithelial cell turnover in relation to ongoing damage of the gastric mucosa in patients with early gastric cancer: increase of cell proliferation in paramalignant lesions

et al. 2005

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“…In renal cell carcinomas, retinoblastoma, or brain gliomas, PIs range from 20% to 28% (Kim et al 1999;Zhang and Takenaka 2000;Zhen et al 2005) and, in Heliobacter-induced epithelial infection leading to cancer, it ranged from 50% to 70% (Unger et al 2001). Skin wound processes lead to a PI of 43% (Amendt et al 2002).…”

Section: Cell Proliferationmentioning

confidence: 99%

Dynamics of cell proliferation and apoptosis reflect different life strategies in hydrothermal vent and cold seep vestimentiferan tubeworms

2009

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Deep-sea vestimentiferan tubeworms, which live in symbiosis with bacteria, exhibit different life strategies according to their habitat. At unstable and relatively short-lived hydrothermal vents, they grow extremely fast, whereas their close relatives at stable and long-persisting cold seeps grow slowly and live up to 300 years. Growth and age differences are thought to occur because of ecological and physiological adaptations. However, the underlying mechanisms of cell proliferation and death, which are closely linked to homeostasis, growth, and longevity, are unknown. Here, we show by immunohistochemical and ultrastructural cell cycle analyses that cell proliferation activities of the two species studied are higher than in any other characterized invertebrate, being only comparable with tumor and wound-healing processes. The slow growth in Lamellibrachia luymesi from cold seeps results from balanced activities of proliferation and apoptosis in the epidermis. In contrast, Riftia pachyptila from hydrothermal vents grows fast because apoptosis is down-regulated in this tissue. The symbiont-housing organ, the trophosome, exhibits a complex cell cycle and terminal differentiation pattern in both species, and growth is regulated by proliferation. These mechanisms have similarities to the up- and down-regulation of proliferation or apoptosis in various types of tumor, although they occur in healthy animals in this study, thus providing significant insights into the underlying mechanisms of growth and longevity.

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Effect of Helicobacter pylori infection and eradication on gastric epithelial cell proliferation and apoptosis

Cited by 14 publications

References 21 publications

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

Epithelial cell turnover in relation to ongoing damage of the gastric mucosa in patients with early gastric cancer: increase of cell proliferation in paramalignant lesions

Dynamics of cell proliferation and apoptosis reflect different life strategies in hydrothermal vent and cold seep vestimentiferan tubeworms

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