In summary (Fig. 8), we report that P. aeruginosa T3SS triggers a rapid phosphorylation cascade involving CrkII/Abl → PKCδ → NLRC4, which leads to caspase-1 activation, culminating in the production of IL-1β and IL-18 pro-inflammatory cytokines, which in turn mobilize inflammatory leukocytes, such as neutrophils (PMNs) and macrophages (Møs), to the site of infection where they combat P. aeruginosa infection. Here, IL1B is linked to infection.