Understanding molecular mechanisms of ()-induced inflammation is important for developing new therapeutic strategies for gastrointestinal diseases. We designed an -neutrophil infection model and explored the effects of infection on neutrophils. infected neutrophils showed a low level of apoptosis. stimulation activated the NACHT/LRR/PYD domain-containing protein 3 (NLRP3)-gasdermin-D (GSDMD) pathway for interleukin (IL)-1β secretion. However, IL-1β secretion was not completely dependent on GSDMD, as inhibition of autophagy significantly reduced IL-1β release, and autophagy-related molecules were significantly upregulated in -infected neutrophils. Therefore, infection inhibits neutrophils apoptosis and induces IL-1β secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against mediated chronic gastritis.