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Methods   The expression of CD86, CD206, and HIF-1 α  in the gastric mucosa was evaluated through immunohistochemistry. RAW 264.7 cells were cocultured with  H. pylori  at various multiplicities of infection (MOIs), and iNOS, CD86, Arg-1, CD206, and HIF-1 α  expression was detected by Western blot, PCR, and ELISA analyses. ROS expression was detected with the fluorescent probe DCFH-DA. Macrophages were also treated with the ROS inhibitor NAC or HIF-1 α  inhibitor YC-1.Results   Immunohistochemical staining revealed that the macrophage polarization state was associated with the progression of gastric lesions and state of  H. pylori  infection. The MOI of  H. pylori  affected macrophage polarization, and  H. pylori  enhanced the expression of ROS and HIF-1 α  in macrophages. A low MOI of  H. pylori  promoted both the M1 and M2 phenotypes, while a high MOI suppressed the M2 phenotype. Furthermore, ROS inhibition attenuated HIF-1 α  expression and switched macrophage polarization from M1 to M2. However, HIF-1 α  inhibition suppressed ROS expression and inhibited both the M1 phenotype and the M2 phenotype. Inhibition of ROS or HIF-1 α  also suppressed the activation of the Akt/mTOR pathway, which was implicated in  H. pylori -induced macrophage polarization.Conclusions   Macrophage polarization is associated with the progression of gastric lesions and state of  H. pylori  infection. The MOI of  H. pylori  influences the macrophage polarization state. Crosstalk between ROS and HIF-1 α  regulates  H. pylori -induced macrophage polarization via the Akt/mTOR pathway.

The Degree of Helicobacter pylori Infection Affects the State of Macrophage Polarization through Crosstalk between ROS and HIF-1α