Disturbance of Apoptosis and DNA Synthesis by Helicobacter pylori Infection of Hepatocytes Academic Article uri icon

abstract

  • We evaluated the effects of infection of hepatocytes with the well-characterized Helicobacter species, H. pylori. Cell number doubled during each 24 h period in mock cultures or following infection with H. pylori 401C (CagA−, VacA−, BabA−, OipA−) (P < 0.05). In contrast, infection with the more virulent H. pylori NCTC11637 (CagA+, VacA+, BabA+, OipA+) resulted in cell arrest (P < 0.05). Furthermore, NCTC11637 activated caspase-3 and increased DNA fragmentation 6.1 ± 1.2 fold (P < 0.01) and the number of apoptotic bodies 9.4 ± 3.5 fold (P < 0.01) compared to controls. The effect was greater than with the less virulent strain 401C (3.8 ± 0.6 fold and 3.9 ± 1.7, respectively, P < 0.05). Strain NCTC11637 at low concentrations increased cellular DNA synthesis 139 ± 6% (P < 0.05) but decreased it to 16 ± 7% (P < 0.01) at high concentrations. In contrast, strain 401C increased DNA synthesis 155 ± 14% of controls (P < 0.05) at high concentrations. The presence of intracellular NCTC11637 within hepatocytes increased DNA fragmentation 3.0 ± 0.4 fold (P < 0.01) greater than in controls. H. pylori infection resulted in strain-species-dependent effects on hepatocytes, and virulent strain caused cell arrest and apoptosis of infected hepatocytes.

publication date

  • January 1, 2008