Up-regulation of human bradykinin B1 receptor by secreted components ofPseudomonas aeruginosavia a NF-κB 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. aeruginosa on the expression of B1R remains unclear, while P. 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. aeruginosa. Components secreted from P. 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-jB signaling pathway in human lung epithelial cells. Taken together, this study demonstrates that P. aeruginosa is capable of upregulating hB1R expression via the NF-jB signaling pathway.

Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9

“…4E) and IKK␤ Ϫ/Ϫ MEFs (Fig. 4F), in which the absence of IKK␤ protein was confirmed as previously reported (18). Taken together, these results suggest that recombinant GroEL induces the expression of PTX3 via the TLR4 and NF-B signaling pathways.…”

Host Cell Responses to Persistent Mycoplasmas - Different Stages in Infection of HeLa Cells with Mycoplasma hominis

“…The complexity of the network is evident from the observation that IL-1 beta upregulates the expression of the bradykinin receptors B1 and B2 [37]. In infection with Listeria, immunity to the bacterium has been shown to be via activation of the BDKRB2 receptor [38] and in infections with Staphylococcus aureus or Pseudomonas aeruginosa , secreted components of the pathogens have been demonstrated to upregulate human BDKRB1 in epithelial cells via NFkB-pathways [39], [40]. Thus, upregulation of the bradykinin receptors B1 and B2 seems to be an important host defense mechanism against invading microbes including M. hominis .…”

Nucleoside Diphosphate Kinase and Flagellin from Pseudomonas aeruginosa Induce Interleukin 1 Expression via the Akt/NF-κB Signaling Pathways

“…NF-B is a key transcriptional factor that initiates host inflammatory responses upon infection by microbes (19). We previously reported that P. aeruginosa activates the NF-B signaling pathway in A549 cells (13). To determine whether cytokine induction by P. aeruginosa strain PAK⌬7 is mediated via the NF-B signaling pathway, we pretreated cells with MG132 (a chemical inhibitor of NF-B) and then exposed them to P. aeruginosa.…”