Up-regulation of bradykinin B2 receptor by Pseudomonas aeruginosa via the NF-κB pathway.

As the first line of host defense, inflammatory responses in response to bacterial infection are initiated by the production of a range of mediators. Infection of Pseudomonas aeruginosa has been shown to stimulate the production of bradykinin (BK), which is known as a universal mediator for the induction of inflammatory reaction via the predominant interaction with the bradykinin B2 receptor (B2R). Thus, the interaction between BK and B2R represents an important host innate response against invading P. aeruginosa. However, the contribution of P. aeruginosa to the up-regulation of B2R expression remains unclear. Here, we report that P. aeruginosa is potent in inducing the expression of B2R at the mRNA and protein levels in a dose- and time-dependent manner. Components produced and secreted from P. aeruginosa could play an essential role in inducing B2R expression, and the secreted components are not under the control of Type III secretion system or quorum sensing. B2R expression in response to P. aeruginosa is mediated by the induction of cellular signaling that leads to the activation of transcription factor NF-κB. Thus, this study demonstrates that P. aeruginosa is able to up-regulate the expression of B2R during infection via the NF-κB signaling pathway.