Proliferative and apoptotic effects of gastric epithelial cells induced by coccoid Helicobacter pylori

Helicobacter pylori exhibit morphology convertion in a spiral or coccoid form. This study aims to reveal the impact of coccoid H. pylori on the proliferation and apoptosis of gastric epithelial cells. The cagA and vacA genes of H. pylori were detected by semi-quantitative RT-PCR. Proliferation and apoptosis were analyzed by the CCK-8 colorimetric method and TUNEL assay, respectively. Egr-1 mRNA and PCNA expression affected by the ERK1/2-specific inhibitor were detected by RT-PCR and immunochemistry. At low density of infection (MOI < 125:1), coccoid H. pylori exerted a stronger effect on proliferation and a weaker effect on apoptosis than did spiral form. The ERK1/2-specific inhibitor significantly blocked the increased expression in Egr-1 and PCNA induced by coccoid H. pylori. Expression of vacA and cagA in coccoid H. pylori decreased compared with the spiral form, whereas vacA decreased more than cagA. The difference of proliferation and apoptosis may be related to the unequal decreased expression of vacA and cagA in coccoid H. pylori. Activation of the ERK1/2-Egr-1-PCNA signal transduction pathway may play an important role in coccoid H. pylori-induced cell proliferation. Long latency of the coccoid form of H. pylori in gastric tissue may be associated with gastric cancer caused by H. pylori.