Abstract: Objective To study the possibility of decidual natural killer(dNK) cells as a potential cell medium in direct contact with trophoblast cells in the maternal-fetal interface through its secreted cytokines, and synergize with pre-eclampsia-associated microRNA-18 a(miR-18 a) affects the infiltration ability of human normal trophoblast cells(HTR8) and participates in the pathogenesis of pre-eclampsia(PE). Methods Of pregnant women with induced abortion from September 2017 to December 2017. Human normal early pregnancy decidual tissue(n=11) was collected, and dNK cells were sorted and purified by gradient density centrifugation combined with flow cytometry. The miR-18 a precursor molecules were transfected into HTR8 cells, which were divided into three groups: miR-18 a expression group, miR-18 a inhibition group and NC group(control group).The dNK was co-cultured with the above three groups of HTR8 cells. The real-time quantitative PCR(RT-qPCR) was used to detect the expression of miR-18 a mRNA in HTR8 cells after transfection. The expression of interleukin 8(IL-8) in the supernatant of each group was detected by ELISA after 24 hours. Transwell experiment was divided into 3 groups: co-culture group, simple culture group and control group. The effect of supernatant obtained from co-culturing of dNK and HTR8 cells on the infiltration ability of trophoblast cells in miR-18 a inhibition group were detected. Results Compared with the control group, miR-18 a overexpression and inhibitory effect was significant(all P<0.001); after co-cultured with dNK and control group HTR8 cells for 24 hours, the expression of IL-8 in the supernatant was lower than that of the control group [(508.35±28.22)ng/L, P<0.001]. Compared with the simple cultured group, the infiltration ability of HTR8 cells in co-cultured group was enhanced(367.11±88.26, P<0.001). Conclusion The dNK cells has certain influence on the infiltration of trophoblast cells through the secretion of the cytokine IL-8; and with the participation of miR-18 a, it may be involved in the pathogenesis of PE.