Objective To investigate the mechanism of expression of the chemokine CCL22 in human normal liverLO2 cells after infected with hepatitis B virus(HBV). Methods LO2 cells were first infected with HBV virus and theexpression of IL-32 was detected by ELISA. Then, exogenous human recombinant IL-32 protein was used to stimulatehuman acute leukemia cell line THP-1 or HEB and THP-1 cells co-cultured with HBV, and TNF-α expression was detectedby ELISA. Second, exogenous human recombinant TNF-α protein was applied for stimulation or co-cultured LO2 and THP-1 cells were infected with HBV. LO2 cells were used to detect the phosphorylation of CREB protein by western blotting withspecific antibody and to detect the expression of the chemokine CCL22 by ELISA. Results HBV induced IL-32 expressionin LO2 cells ( P < 0. 05),and virus-induced IL-32 in turn induced the secretion of TNF-α by THP-1 cells ( P < 0. 05).TNF-α induced activation of the CREB pathway in LO2 cells. This activation then promoted the expression of the chemokineCCL22 in LO2 cells ( P < 0. 05). Conclusions LO2 cells co-cultured under conditions of HBV infection and in thepresence of THP-1 can express CCL22. The mechanism behind this may involve HBV inducing IL-2 expression in LO2cells, and then IL-32 induces the secretion of TNF-α by THP-1 cells, after which TNF-α promotes the HBV-infection. LO2 cells to express chemokine CCL22.