Gram-negative pathogens such as S. Typhimurium and EPEC use T3SS to inject virulence factors such as EspT and SpiC that activate NF-κB to induce COX-2 expression. This activation of COX-2, in turn, leads to the production of prostaglandins, such as PGE2, which act via discrete EP receptors EP2 and EP4 to enhance inflammasome activation during pyroptosis. Inflammasome activation further drives the formation of PITs, which trap live bacteria. Neutrophils are recruited to the site of infection via eicosanoids and phagocytize PITs to clear the invaders.