Our present results revealed severe disease phenotype, increased C. difficile burden and decreased IL-1β production after the inhibition of caspase-1 during in vivo infection, suggesting that caspase-1-dependent inflammasome plays an important role in the host response during CDI and impaired bacterial clearance is the major cause of severe disease progression of CDI. The gene discussed is IL1B; the disease is clostridium difficile infection.