Collectively, these findings provide compelling, multi-dimensional evidence that selective inhibition of Caspase-1 and Caspase-11 not only suppresses EV71-induced neuroinflammation in a targeted manner but also exerts robust protective effects on brain tissue, with this dual outcome primarily mediated by blocking the maturation and extracellular release of the pro-inflammatory cytokines IL-1β and IL-18—an effect that disrupts the “viral infection-inflammation-pyroptosis” pathogenic cascade underlying EV71-associated neurological injury. Here, IL1B is linked to viral infectious disease.