scholarly journals WS22.5 Effect of the Burkholderia cenocepacia exoproteome on CFTR protein expression in human cystic fibrosis lung epithelial cell models

2013 ◽  
Vol 12 ◽  
pp. S47
Author(s):  
S. Canato ◽  
M. Telhada ◽  
M.D. Amaral ◽  
L. Clarke
2009 ◽  
Vol 61 (5) ◽  
pp. 583-591 ◽  
Author(s):  
Sibylle Endter ◽  
Danielle Francombe ◽  
Carsten Ehrhardt ◽  
Mark Gumbleton

2014 ◽  
Vol 83 (2) ◽  
pp. 812-821 ◽  
Author(s):  
Ana S. Ferreira ◽  
Inês N. Silva ◽  
Fábio Fernandes ◽  
Ruth Pilkington ◽  
Máire Callaghan ◽  
...  

Bacterial tyrosine kinases and their cognate protein tyrosine phosphatases are best known for regulating the biosynthesis of polysaccharides. Moreover, their roles in the stress response, DNA metabolism, cell division, and virulence have also been documented. The aim of this study was to investigate the pathogenicity and potential mechanisms of virulence dependent on the tyrosine kinase BceF and phosphotyrosine phosphatase BceD of the cystic fibrosis opportunistic pathogenBurkholderia contaminansIST408. The insertion mutantsbceD::Tp andbceF::Tp showed similar attenuation of adhesion and invasion of the cystic fibrosis lung epithelial cell line CFBE41o- compared to the parental strainB. contaminansIST408. In the absence ofbceDorbceFgenes,B. contaminansalso showed a reduction in the ability to translocate across polarized epithelial cell monolayers, demonstrated by a higher transepithelial electrical resistance, reduced flux of fluorescein isothiocyanate-labeled bovine serum albumin, and higher levels of tight junction proteins ZO-1, occludin, and claudin-1 present in monolayers exposed to these bacterial mutants. Furthermore,bceD::Tp andbceF::Tp mutants induced lower levels of interleukin-6 (IL-6) and IL-8 release than the parental strain. In conclusion, although the mechanisms of pathogenicity dependent on BceD and BceF are not understood, these proteins contribute to the virulence ofBurkholderiaby enhancement of cell attachment and invasion, disruption of epithelial integrity, and modulation of the proinflammatory response.


2009 ◽  
Vol 61 (5) ◽  
pp. 583-591 ◽  
Author(s):  
Sibylle Endter ◽  
Danielle Francombe ◽  
Mark Gumbleton ◽  
Carsten Ehrhardt

2011 ◽  
Vol 60 (3) ◽  
pp. 289-299 ◽  
Author(s):  
Anne Costello ◽  
Gillian Herbert ◽  
Lydia Fabunmi ◽  
Kirsten Schaffer ◽  
Kevin A. Kavanagh ◽  
...  

Pandoraea species have emerged as opportunistic pathogens among cystic fibrosis (CF) and non-CF patients. Pandoraea pulmonicola is the predominant Pandoraea species among Irish CF patients. The objective of this study was to investigate the pathogenicity and potential mechanisms of virulence of Irish P. pulmonicola isolates and strains from other Pandoraea species. Three patients from whom the P. pulmonicola isolates were isolated have since died. The in vivo virulence of these and other Pandoraea strains was examined by determining the ability to kill Galleria mellonella larvae. The P. pulmonicola strains generally were the most virulent of the species tested, with three showing a comparable or greater level of virulence in vivo relative to another CF pathogen, Burkholderia cenocepacia, whilst strains from two other species, Pandoraea apista and Pandoraea pnomenusa, were considerably less virulent. For all Pandoraea species, whole cells were required for larval killing, as cell-free supernatants had little effect on larval survival. Overall, invasive Pandoraea strains showed comparable invasion of two independent lung epithelial cell lines, irrespective of whether they had a CF phenotype. Pandoraea strains were also capable of translocation across polarized lung epithelial cell monolayers. Although protease secretion was a common characteristic across the genus, it is unlikely to be involved in pathogenesis. In conclusion, whilst multiple mechanisms of pathogenicity may exist across the genus Pandoraea, it appears that lung cell invasion and translocation contribute to the virulence of P. pulmonicola strains.


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