Journal of Gastroenterology

, Volume 40, Issue 3, pp 236–246

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

  • Kyoko Ozawa
  • Seiichi Kato
  • Hitoshi Sekine
  • Tomoyuki Koike
  • Takanori Minoura
  • Kazuie Iinuma
  • Hiroshi Nagura
Article

DOI: 10.1007/s00535-004-1530-7

Cite this article as:
Ozawa, K., Kato, S., Sekine, H. et al. J Gastroenterol (2005) 40: 236. doi:10.1007/s00535-004-1530-7

Abstract

Background

In adults, epithelial cell proliferation and apoptosis of the gastric mucosa are induced by Helicobacter pylori infection and are associated with gastric atrophy or gastric carcinoma. In children, there are few studies about such epithelial changes. To elucidate the role of H. pylori infection in gastric mucosal inflammation, we immunohistochemically examined gastric mucosa of Japanese children.

Methods

Biopsy specimens obtained from the gastric antrum and corpus of H. pylori-infected (n = 13) and noninfected children (n = 15) were studied for immunolocalization of Ki-67, single-strand DNA, manganese superoxide dismutase (Mn-SOD), and CD68, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling. In 10 patients with successful eradication, pre- and posttreatment results were compared.

Results

In both gastric antrum and corpus, neutrophil and mononuclear cell infiltration, epithelial cell proliferation, and apoptosis significantly increased in H. pylori-infected patients, predominantly in the antrum. In the antrum of H. pylori-infected patients, there was positive correlation between the degrees of neutrophil infiltration and cell proliferation (P < 0.05) or apoptosis (P < 0.05). H. pylori eradication improved mucosal inflammation, cell proliferation (P < 0.001), and apoptosis (P < 0.01) in the antrum. Mn-SOD immunoreactivity and CD68-positive macrophages in the antrum, which significantly increased in H. pylori-infected patients, decreased after the eradication.

Conclusions

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.

Key words

Helicobacter pylori cell proliferation apoptosis superoxide dismutase children 

Copyright information

© Springer-Verlag Tokyo 2005

Authors and Affiliations

  • Kyoko Ozawa
    • 1
    • 2
  • Seiichi Kato
    • 1
  • Hitoshi Sekine
    • 3
  • Tomoyuki Koike
    • 3
  • Takanori Minoura
    • 1
  • Kazuie Iinuma
    • 1
  • Hiroshi Nagura
    • 2
    • 4
  1. 1.Department of PediatricsTohoku University School of MedicineSendaiJapan
  2. 2.Department of PathologyTohoku University School of MedicineSendaiJapan
  3. 3.Department of GastroenterologyTohoku University School of MedicineSendaiJapan
  4. 4.Department of PathologySendai Shakaihoken HospitalSendaiJapan

Personalised recommendations