〔Abstract〕 Objective To investigate the role of chloride intracellular channels(CLICs) in inflammasome activation duringL.monocytogenesinfection. Methods The primary cultured murine bone marrow macrophages were treated with CLIC inhibitor IAA94 and infected withL.monocytogenes, the levels of interleukin-1 beta(IL-1β) in cell culture supernatants and cell lysates were detected using ELISA and Western blot, respectively. Results The release of IL-1β and lactate dehydrogenase(LDH) decreased in the group of indanyloxyacetic acid 94(IAA94) treatment withL.monocytogenesinfection. Western blot showed that the level of IL-1β in the cell lysates with IAA94 treatment andL.monocytogenesinfection decreased but not in Nod-like receptor family, pyrin domain containing 3(NLRP3) dependent manner. Conclusion Chloride channel proteins is essential in inflammasome activation duringL.monocytogenesinfection, but it may not be in NLRP3-independent way, and the mechanism is still to be further elucidated.