10.3389/fmicb.2018.03018.s002
Yi-Chia Liu
Yi-Chia
Liu
Farah Hussain
Farah
Hussain
Ola Negm
Ola
Negm
Ana Pavia
Ana
Pavia
Nigel Halliday
Nigel
Halliday
Jean-Frédéric Dubern
Jean-Frédéric
Dubern
Sonali Singh
Sonali
Singh
Sirina Muntaka
Sirina
Muntaka
Lee Wheldon
Lee
Wheldon
Jeni Luckett
Jeni
Luckett
Paddy Tighe
Paddy
Tighe
Cynthia Bosquillon
Cynthia
Bosquillon
Paul Williams
Paul
Williams
Miguel Cámara
Miguel
Cámara
Luisa Martínez-Pomares
Luisa
Martínez-Pomares
Data_Sheet_2_Contribution of the Alkylquinolone Quorum-Sensing System to the Interaction of Pseudomonas aeruginosa With Bronchial Epithelial Cells.PDF
Frontiers
2018
bronchial epithelial cells
Pseudomonas aeruginosa
quorum sensing
inflammation
pseudomonas quinolone signal
2018-12-18 12:28:03
Dataset
https://frontiersin.figshare.com/articles/dataset/Data_Sheet_2_Contribution_of_the_Alkylquinolone_Quorum-Sensing_System_to_the_Interaction_of_Pseudomonas_aeruginosa_With_Bronchial_Epithelial_Cells_PDF/7478489
<p>Pseudomonas aeruginosa causes infections in patients with compromised epithelial barrier function. Multiple virulence factors produced by P. aeruginosa are controlled by quorum sensing (QS) via 2-alkyl-4(1H)-quinolone (AQ) signal molecules. Here, we investigated the impact of AQs on P. aeruginosa PAO1 infection of differentiated human bronchial epithelial cells (HBECs). The pqsA-E operon is responsible for the biosynthesis of AQs including the 2-alkyl-3-hydroxy-4-quinolones, 4-hydroxy-2-alkylquinolines, and 4-hydroxy-2-alkylquinoline N-oxides as exemplified by pseudomonas quinolone signal (PQS), 2-heptyl-4-hydroxyquinoline (HHQ), and 2-heptyl-4-hydroxyquinoline N-oxide (HQNO), respectively. PQS and HHQ both act as QS signal molecules while HQNO is a cytochrome inhibitor. PqsE contributes both to AQ biosynthesis and promotes virulence in a PQS-independent manner. Our results show that PQS, HHQ, and HQNO were produced during PAO1 infection of HBECs, but no differences in growth or cytotoxicity were apparent when PAO1 and an AQ-negative ΔpqsA mutant were compared. Both strains promoted synthesis of inflammatory cytokines TNF-α, interleukin (IL)-6, and IL-17C by HBECs, and the provision of exogenous PQS negatively impacted on this response without affecting bacterial growth. Expression of pqsE and the PQS-independent PqsE-regulated genes mexG and lecA was detected during HBEC infection. Levels were reduced in the ΔpqsA mutant, that is, in the absence of PQS, and increased by exogenous PQS. These results support an AQ-independent role for PqsE during initial infection of HBEC by P. aeruginosa and for PQS as an enhancer of PqsE and PqsE-controlled virulence determinants and as an immunomodulator.</p>