Helicobacter pylori protects oncogenically transformed cells from reactive oxygen species-mediated intercellular
Georg Bauer1, Stefan Bereswill2, Peter Aichele3
1Institute of Virology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg D-79104, Germany, Institute of Medical Microbiology, Charité, Berlin D-12203, Germany and Institute of Immunology and Institute of Microbiology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg D-79104, Germany georg.bauer@uniklinik-freiburg.de.
Abstract:
Malignant transformation of gastric epithelial cells by chronic Helicobacter pylori infection is caused by several mechanisms including attraction of reactive oxygen species (ROS)-producing neutrophils and cytotoxin-associated antigen A-mediated dysplastic alterations. Here we show that H.pylori protects transformed cells from ROS-mediated intercellular induction of apoptosis. This potential control step in oncogenesis depends on the HOCl and NO/peroxynitrite (PON) signaling pathways. Helicobacter pylori-associated catalase and superoxide dismutase (SOD) efficiently cooperate in the inhibition of HOCl and the NO/PON signaling pathways. Helicobacter pylori catalase prevents HOCl synthesis through decomposition of hydrogen peroxide. Helicobacter pylori-associated SOD interferes with the crucial interactions between superoxide anions and HOCl, as well as superoxide anions and NO. The ratio of bacteria to malignant cells is critical for sufficient protection of transformed cells. Low concentrations of H.pylori more efficiently inhibited ROS-mediated destruction of transformed cells when compared with high concentrations of bacteria. Our data demonstrate the critical role of H.pylori antioxidant enzymes in the survival of transformed cells, modulating an early step of oncogenesis that is distinct from the transformation process per se.
More Related Videos
Related Concept Videos
Abnormal Proliferation
The Intrinsic Apoptotic Pathway
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...


