IMR Press / FBL / Volume 6 / Issue 4 / DOI: 10.2741/shirin

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Effects of H. pylori infection of gastric epithelial cells on cell cycle control

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1 Department of Gastroenterology, The E. Wolfson Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Israel
2 Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons of Columbia University, New York, NY
3 Department of Medicine, Division of Gastroenterology, Rhode Island Hospital/Brown University, Providence, RI
Front. Biosci. (Landmark Ed) 2001, 6(4), 104–118;
Published: 1 October 2001

Chronic infection of the gastric mucosa by the bacterium H. pylori results in an intense inflammatory response which can last for decades. An associated host response is a chronic hyperproliferative state, in which there is increased cell turnover and also increased apoptosis of the gastric epithelial cells. Recent studies have also demonstrated abnormalities in the expression of cell cycle control proteins. This review describes these events, emphasizing recent studies on the effects of H. pylori infection on cell cycle progression and the expression of cell cycle regulatory proteins. The systems that have been studied include in vivo studies in humans and in experimental animals, and in vitro studies in which gastric epithelial cells were co-cultivated with H. pylori. The earliest event following H. pylori's interaction with epithelial cells appears to be growth inhibition and apoptosis. The hyperproliferative response observed in the gastric mucosa is secondary to this initial insult and is associated with increased expression of cyclin D1, the cyclin dependent kinase inhibitor p16ink4a and of p53 and decreased expression of the cyclin dependent kinase inhibitor p27kip1. Dysregulation of the hyperproliferative response may, ultimately, be responsible for the ability of H. pylori to enhance the development of gastric cancer.

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