title: Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection.
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.
authors.affiliation: Department of Pediatrics, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Ozawa
authors.forename: Seiichi
authors.initials: S
authors.lastname: Kato
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sekine
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Koike
authors.forename: Takanori
authors.initials: T
authors.lastname: Minoura
authors.forename: Kazuie
authors.initials: K
authors.lastname: Iinuma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagura
mesh_terms: D000293:Adolescent; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D017209:Apoptosis / Q000235:genetics / Q000276:immunology; D049109:Cell Proliferation; D002648:Child; D004249:DNA Damage; D004847:Epithelial Cells / Q000201:enzymology / Q000276:immunology / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology*; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007564:Japan / Q000453:epidemiology; D008297:Male; D011379:Prognosis; D012189:Retrospective Studies; D013482:Superoxide Dismutase / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D013482:Superoxide Dismutase; C067980:CD68 antigen, human; D000097382:CD68 Molecule