P. aeruginosa biofilm activates the NLRP3 inflammasomes in vitro

The ability of P.aeruginosa to form biofilms renders common treatments inefficient, thereby promoting chronic infection. Inflammasomes activate caspase-1, which is important for the maturation of IL-1 beta and IL-18 and evoke an inflammatory response. We aimed to investigate the activation of inflammasomes induced by P.aeruginosa biofilm. THP-1 cells were mock-infected or infected with PAO1 biofilms. Protein levels of caspase-1 p20, procaspase-1, caspase-4 p20, and pro-caspase-4 in THP-1 macrophages were determined by Western blotting. The expression of NLRC4 and NLRP3 was measured by RT-PCR. The production of IL-1 beta and IL-18 was monitored using ELISA. P. aeruginosa biofilm significantly elevated caspase-1 levels, and decreased NLRC4 levels. Additionally, caspase-4 and NLRP3 levels were significantly increased. P.aeruginosa biofilm significantly enhanced IL 1 beta and IL-18 production. We concluded that P. aeruginosa biofilm induced the production of IL-1 beta and IL-18, possibly via NLRP3 inflammasomes, rather than NLRC4 inflammasomes.

Automated summary

The ability of P.aeruginosa biofilms to activate inflammasomes and increase inflammatory response contributes to chronic infection. This study found that P.aeruginosa biofilms significantly enhance the production of IL-1β and IL-18, possibly through the regulation of NLRP3 inflammasomes rather than NLRC4 inflammasomes.