@article{4e30071eb81442bab45caf79cda2eea9,
title = "Epithelial cell kinetics of the gastric mucosa during Helicobacter pylori infection.",
abstract = "Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load and cytokines which may improve knowledge concerning the outcome of gastric diseases caused by H. pylori. Antral biopsies from 42 dyspeptic patients including 27 H. pylori-positive and 15 H. pylori-negative patients were tested for apoptotic activity by the TUNEL assay, and immuno-histochemically for p53 and the proliferative marker Ki-67. H. pylori infection, bacteria load and inflammatory activity were associated with increased cell turnover as judged by enhanced activities of TUNEL, p53 and Ki-67. Only p53 was significantly correlated to IFN-gamma, IL-8 and IL-10. The H. pylori-positive state was furthermore accompanied by varying degrees of altered distribution pattern of the markers studied, with occasional presence of apoptosis in the deeper pit zones, upward extension of Ki-67 and to a lesser degree of p53. Given a similar pattern of change in proliferation and apoptosis in some neoplastic lesions in other parts of the gastrointestinal tract, such studies in cell turnover may provide insights valuable in the investigations of potential precursors of gastric malignancies.",
keywords = "helicobacter pylori, gastritis, mavekatar, maves{\aa}r, ulcus ventriculi, gastric ulceration, inflammation, malignancies",
author = "Susanne Holck and I.L. Holm and P.P. Holck and M. Pedersen and S. Norn and H. Permin and A. N{\o}rgaard and L.P. Andersen",
year = "2007",
doi = "10.1111/j.1574-695X.2007.00254.x",
language = "English",
volume = "50",
pages = "206--212",
journal = "F E M S Immunology and Medical Microbiology",
issn = "0928-8244",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "2",
}