Up-regulation of human bradykinin B1 receptor by secreted components of Pseudomonas aeruginosa via a NF-?B pathway in epithelial cells

Abstract

Pulmonary epithelial cells produce neutrophil chemotactic activity in response to pathogenic bacterial infections, resulting in neutrophil migration to infection sites. Elicited neutrophils in the inflamed tissues were found to be dependent on bradykinin B1 receptor (B1R), which shows high affinity for the active metabolites derived from bradykinin. Thus, the up-regulation of bradykinin and B1R expression represents an important host defense response against invading microbes such as Pseudomonas aeruginosa. However, the effect of P.similar to aeruginosa on the expression of B1R remains unclear, while P.similar to aeruginosa infection is known to stimulate the production of bradykinin. Here, we report that human B1R (hB1R) transcription is up-regulated in host cells co-cultured with P.similar to aeruginosa. Components secreted from P.similar to aeruginosa play a major role in the up-regulation, and the secretion of the components is not controlled by either type III secretion system or quorum sensing. Moreover, the B1R induction is mediated by a NF-kappa B signaling pathway in human lung epithelial cells. Taken together, this study demonstrates that P.similar to aeruginosa is capable of up-regulating hB1R expression via the NF-kappa B signaling pathway.