Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection.
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.
Ozawa
Kyoko
K
Department of Pediatrics, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Kato
Seiichi
S
Sekine
Hitoshi
H
Koike
Tomoyuki
T
Minoura
Takanori
T
Iinuma
Kazuie
K
Nagura
Hiroshi
H
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
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D013482:Superoxide Dismutase; C067980:CD68 antigen, human; D000097382:CD68 Molecule