P. aeruginosa is an opportunistic human pathogen associated with cystic fibrosis.  In P. aeruginosa infections, quorum sensing is critical for biofilm formation and pathogenicity.   P. aeruginosa contains two pairs of LuxI/LuxR homologs, LasI/LasR and RhlI, RhlR.   LasI and RhlI are synthase enzymes that catalyze the synthesis of N-(3-oxododecanoyl)-homoserine lactone and N-(butyryl)-homoserine lactone, respectively.  The LasI/LasR and the RhlI/RhlR circuits function in tandem to regulate the expression of a number of virulence genes.  At a threshold concentration, LasR binds N-(3-oxododecanoyl)-homoserine lactone.  Together this bound complex promotes the expression of virulence factors that are responsible for early stages of the infection process.
LasR bound by its autoinducer also activates the expression of the RhlI/RhlR system in P. aeruginosa.  This causes the expression of RhlR which then binds its autoinducer, N-(butryl)-homoserine lactone.  In turn, autoinducer-bound RhlR activates a second class of genes involved in later stages of infection, including genes needed for antibiotic production.  Presumably, antibiotic production by P. aeruginosa is used to prevent opportunistic infections by other bacterial species.  N-(3-oxododecanoyl)-homoserine lactone prevents binding between N-(butryl)-homoserine lactone and its cognate regulator, RhlR.  It is believed that this control mechanism allows P. aeruginosa to initiate the quorum-sensing cascades sequentially and in the appropriate order so that a proper infection cycle can ensue.