title: [Gastric epithelial cell proliferation, apoptosis and P53 protein expression in children with Helicobacter pylori associated chronic gastritis].
abstract: OBJECTIVE
  To investigate whether Helicobacter pylori infection has any effects on the epithelial cell proliferation, apoptosis and P53 gene expression as well as its role in the pathogenesis of chronic gastritis.
  
  
  METHODS
  Sixty children with chronic gastritis were studied. All the children underwent upper digestive tract endoscopy and biopsy specimens were taken. Helicobacter pylori infection was determined with microscopic examination after Gimsa staining and the rapid urease test and 30 of the children were Helicobacter pylori positive and the other 30 were negative. The relation between the findings and cell proliferation was studied by immunostaining; the status of gastric apoptosis was tested by DNA fragmentation in situ using TdT-mediated dUTP biotin nick end labeling (TUNEL). Immunohistochemical method was used to detect the expression of P53 protein; CagA antibody was tested by Western blotting.
  
  
  RESULTS
  (1) The proliferative index and apoptosis index in children with Helicobacter pylori infection with CagA positive gastritis were much higher than those of Helicobacter pylori negative gastritis patients [(11.56 +/- 4.21)% vs. (5.85 +/- 2.21)%, (10.58 +/- 5.31)% vs. (2.86 +/- 0.64)%, P < 0.01]. (2) The proliferative index and apoptosis index in 30 cases with Helicobacter pylori infection with CagA positive gastribis were much higher than 21 cases who were cured by effective drugs [(11.50 +/- 4.11)% vs. (3.74 +/- 2.30)%; (10.58 +/- 4.02)% vs. (3.74 +/- 2.30)%, P < 0.01]. (3) The expression of P53 protein in Helicobacter pylori with CagA positive gastritis children was much higher than that of Helicobacter pylori negative cases [(63% vs 16%), P < 0.1].
  
  
  CONCLUSIONS
  CagA positive Helicobacter pylori infection with gastritis improved gastric epithelial cell proliferation and apoptosis. The abnormal expression of P53 protein in gastric epithelium may play an important role in regulation of the processes.
authors: Department of Gastroenterology, Guiyang Children's Hospital, Guiyang 550003, China.
authors: Li
authors: L
authors: Zhu
authors: Rong
authors: R
authors: Jin
authors: Hong-juan
authors: HJ
authors: Wang
authors: Hui
authors: H
authors: Li
authors: Quan
authors: Q
authors: Zhan
authors: Wen-li
authors: WL
authors: Liu
authors: Xiao-li
authors: XL
authors: Quan
mesh_terms: D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology; D017209:Apoptosis; D001426:Bacterial Proteins / Q000276:immunology; D001706:Biopsy; D049109:Cell Proliferation; D002648:Child; D002675:Child, Preschool; D004847:Epithelial Cells / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000150:complications / Q000473:pathology*; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D020287:In Situ Nick-End Labeling; D008297:Male; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016159:Tumor Suppressor Protein p53; C080866:cagA protein, Helicobacter pylori