Vibrio harveyi,an important zoonotic pathogen,can infect wounds and cause inflammatory response.Understanding the inflammatory response pathways could facilitate the exploration of molecular mechanisms for treating V.harveyi infection.NLR family pyrin domain-containing 3 (NLRP3) inflammasome is involved in the interaction between hosts and pathogenic microor-ganisms and could be sensed by various pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs).Nonetheless,the function of NLRP3 inflamma-some in V.harveyi infection remains unclear.In the present study,we established a V.harveyi infection model using murine peritoneal macrophages (PMs).Various techniques,including west-ern blot analysis,enzyme-linked immunosorbent assay (ELISA),RT-qPCR,immunofluorescence,and inhibition assays,were used to explore the molecular mechanism of V.harveyi-induced inflam-mation.The results showed that many inflammatory cytokines participated in V.harveyi infection,with interleukin (IL)-1β being the most abundant.Pan-caspase inhibitor pretreatment significantly decreased the secretion of IL-1β in murine PMs.Moreover,the identification of V.harveyi involved a large number of NLR molecules,especially the NLRP3 receptor,and further studies revealed that NLPR3 inflammasome was activated by V.harveyi infection,as evidenced by puncta-like NLRP3 surrounding Cell nuclear,ASC specks in the nucleus and cytoplasm,and ASC oligomerization.Inhi-bition of NLRP3 inflammasome impaired the release of mature IL-1β in V.harveyi-infected murine PMs.Furthermore,blocking the secretion of mature IL-1β could markedly decrease the release of other proinflammatory cytokines,including IL-6,IL-12,and tumor necrosis factor-α.Overall,these data indicated that NLRP3 inflammasome was activated in response to V.harveyi infection and enhanced inflammatory response by promoting IL-1β secretion in murine PMs.