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Pseudomonas aeruginosa Attenuates Inflammasome Activation via Quorum Sensing‐Dependent Mechanism

Quorum sensing (QS) is a bacterial communication mechanism that promotes coordinated adaptation by triggering expression of a wide range of genes. QS is thought to strongly contribute to the virulence of Pseudomonas aeruginosa, an opportunistic bacterial pathogen, but the molecular effect of QS on host inflammasome defense is completely unknown. Here, we present evidence that P. aeruginosa dampens host inflammasome signaling by QS‐related products in mouse bone marrow‐derived macrophages. We demonstrate that QS‐regulated virulence factor pyocyanin and QS autoinducer 3‐oxo‐C12‐homoserine lactone directly suppress NLRC4‐ and NLRP3‐mediated inflammasome assembly and activation. In addition, bacteria‐free secretant from QS‐defective ΔlasR/rhlR mutant, but not from wild type bacteria, induces robust activation of the NLRC4 inflammasome. Extracellular P. aeruginosa‐released flagellin might be responsible for this inflammasome activation by ΔlasR/rhlR secretant, but QS‐dependent secretion of bacterial proteases degrade extracellular flagellin to evade NLRC4 inflammasome activation. P. aeruginosa–secreted proteases also impair inflammasome components and pro‐inflammatory cytokines in the extracellular space. Taken together, our data indicate that QS system of P. aeruginosa facilitates bacteria to evade host inflammasome‐dependent sensing machinery.