A QseBC-like system is involved in motility and biofilm formation responses to catecholamines in Pseudomonas aeruginosa PAO1.

Catecholamines hormones, including epinephrine (Epi), norepinephrine (NE), and dopamine (Dopa), are known to enhance Pseudomonas aeruginosa PAO1 growth, motility, and biofilm formation. However, the bacterial sensing mechanisms underlying these responses remain poorly understood. In this study, adrenergic and dopaminergic inhibitors (phentolamine, propranolol and chlorpromazine) were used to investigate how P. aeruginosa PAO1 recognizes host-derived catecholamines. We found that phentolamine and propranolol inhibited Epi/NE-induced bacterial growth, motility and biofilm formation. In contrast, chlorpromazine selectively abolished Dopa-induced biofilm formation. These results suggest the involvement of at least one putative adrenergic/dopaminergic-like sensor in P. aeruginosa PAO1. Bioinformatics analysis identified PmrB, a QseC-like histidine sensor kinase in PmrAB two-component system (TCS), as a plausible candidate. Molecular docking using an AlphaFold3 model of PmrB, showed that catecholamines can bind to a cavity at the dimer interface. A ΔpmrAB mutant failed to respond to catecholamine exposure in motility and biofilm experiments, supporting a direct role of the PmrAB TCS in mediating PAO1 responses to host-derived catecholamines.