〔Abstract〕 Objective To explore whether the NLRP3 inflammasome is activated after Newcastle disease virus (NDV) exposure to esophageal cancer ECA109 cells, whether its activation is related to K+efflux, and the effect of ATP/P2X7 axis on the activation of NLRP3 inflammasome.Methods The expression of NLRP3 and IL-1β was detected by Western blot; the content of IL-1β in the supernatant was detected by ELISA; the formation of ASC spots was detected by fluorescence immunoassay; the change of intracellular K+concentration was detected by fluorescent probe technology; Interventions with ATPase, ATP and P2X7 receptor inhibitors were used to investigate their role in NLRP3 inflammasome activation.Results Compared with the control group, the expression of NLRP3, IL-1β and ASC protein in cells was up-regulated after NDV F3 infection; the intracellular potassium concentration decreased with the prolongation of infection time(P<0. 05). After the intervention of P2X7 receptor inhibitor, the efflux of intracellular K+was blocked. With the increase of inhibitor concentration, the efflux of K+was maximally inhibited at 10 μmol/L(P<0. 05). The results of ATPase and ATP intervention showed that ATPase inhibited K+efflux, while ATP promoted K+efflux. Western blot results showed that compared with the control group, P2X7 receptor was inhibited, and the expressions of NLRP3 and IL-1β were down-regulated; after ATPase intervened cells, the expressions of NLRP3 and IL-1β decreased; After ATP intervention in cells, the protein expressions of NLRP3 and IL-1β were up-regulated(P<0. 05).Conclusion NDV F3 infection of ECA109 cells can activate the NLRP3 inflammasome,the mechanism may be related to the ATP/P2X7 axis.