A model of Helicobacter infection using an artificial liver constructed by a radial-flow bioreactor.

Helicobacter DNA has been detected in liver tissues from patients with hepatocellular carcinoma and other liver diseases, suggesting a potential involvement of Helicobacter infection in hepatic pathogenesis. However, whether Helicobacter pylori (H. pylori) can infect human hepatocytes and how such infection affects hepatocyte structure and function remain unclear. In this study, we used a three-dimensional (3D) bioartificial liver model reconstructed using radial-flow bioreactor technology to investigate the ability of H. pylori to infect hepatocytes and to characterize the cellular responses induced by infection. Histological analysis and electron microscopy demonstrated that H. pylori adhered to the hepatocyte surface and penetrated intercellular spaces. Infection significantly induced a threefold increase in apoptosis, accompanied by upregulation of TNF-α (1.5-fold) and activation of NF-κB (1.6-fold) (all P < 0.05). In addition, PCNA expression significantly decreased to approximately 60% of control levels (P < 0.05), whereas Akt activation was enhanced and β-catenin was predominantly localized in the cytoplasm. No significant differences were observed in Ki-67, IL-8, Ets-1, or c-Met expression compared with controls. These findings demonstrate that H. pylori can infect the 3D liver model and induce apoptosis and signaling alterations in hepatocytes, suggesting a potential pathological impact on the liver. Further studies are required to determine whether similar effects occur in the human liver in vivo.