Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection

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Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection

NL Jones, PT Shannon, E Cutz, H Yeger and PM Sherman
Research Institute, The Hospital for Sick Children, and the Department of Pediatrics, University of Toronto, Ontario, Canada.

Childhood acquisition of Helicobacter pylori is a critical risk factor for gastric cancer. Since tumorigenesis involves deregulation of proliferation and apoptosis, we examined gastric epithelial cell proliferation and apoptosis in H. pylori-infected children. Apoptosis and proliferation of gastric antral epithelial cells in biopsy specimens from patients with H. pylori-induced gastritis, secondary gastritis, and noninflamed controls were compared. p53 protein expression was examined immunohistochemically. Apoptotic cells were identified in the surface epithelium in each group. The apoptotic index was higher in specimens from patients with H. pylori gastritis (120 +/- 10) than secondary gastritis (50 +/- 10) and noninflamed controls (40 +/- 10, analysis of variance P < 0.005). Apoptosis decreased following H. pylori eradication and resolution of gastritis (P < 0.02). An expanded proliferative compartment was identified in H. pylori-induced gastritis (32.4 +/- 3.5; proliferative labeling index +/- SE) compared with secondary gastritis (18.9 +/- 2.8) and noninflamed controls (13.7 +/- 3.1, analysis of variance P < 0.01). The accelerated cell turnover was associated with p53 overexpression (analysis of variance P < 0.005). Accumulation of p53 was not associated with expression of the cyclin-dependent kinase inhibitor p21. The occurrence of altered cell turnover early in the natural history of chronic infection provides an explanation for the increased risk of gastric cancer development associated with childhood acquisition of infection.

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				C. Basak, S. K. Pathak, A. Bhattacharyya, S. Pathak, J. Basu, and M. Kundu The Secreted Peptidyl Prolyl cis,trans-Isomerase HP0175 of Helicobacter pylori Induces Apoptosis of Gastric Epithelial Cells in a TLR4- and Apoptosis Signal-Regulating Kinase 1-Dependent Manner J. Immunol., May 1, 2005; 174(9): 5672 - 5680. [Abstract] [Full Text] [PDF]

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				S. Backert, T. Schwarz, S. Miehlke, C. Kirsch, C. Sommer, T. Kwok, M. Gerhard, U. B. Goebel, N. Lehn, W. Koenig, et al. Functional Analysis of the cag Pathogenicity Island in Helicobacter pylori Isolates from Patients with Gastritis, Peptic Ulcer, and Gastric Cancer Infect. Immun., February 1, 2004; 72(2): 1043 - 1056. [Abstract] [Full Text] [PDF]

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Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection

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