Our findings indicating the interplay between the activities of NSPs and caspase-1 regulates IL-1β secretion become relevant not only in relation to E. coli infections but also regarding human neutrophil proinflammatory capacity, because together with our previous results with LPS+ATP, it shows that a common mechanism controls the intensity of IL-1β response avoiding the excessive release of this extremely proinflammatory cytokine. Here, CASP1 is linked to escherichia coli infection.