We reported that NLRP3 is transcribed de novo in neutrophils in response to NFκB-activating mediators4; it is therefore likely that in the absence of priming by LPS, a 3 h PAO1 infection at a 10:1 multiplicity of infection does not induce sufficient NLRP3 expression in bone marrow neutrophils, leaving NLRC4 as the default inflammasome sensor responding to P. aeruginosa. This evidence concerns the gene NLRC4 and infection.