Pseudomonas aeruginosa strains from the chronically infected cystic fibrosis lung display increased invasiveness of A549 epithelial cells over time

2012 ◽  
Vol 53 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Christopher J. Harmer ◽  
James A. Triccas ◽  
Honghua Hu ◽  
Barbara Rose ◽  
Peter Bye ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Cystic Fibrosis Lung ◽  
Over Time

scholarly journals Nonclassical Pathway of Pseudomonas aeruginosa DNA-Induced Interleukin-8 Secretion in Cystic Fibrosis Airway Epithelial Cells

2006 ◽  
Vol 74 (5) ◽  
pp. 2975-2984 ◽  
Author(s):  
Mónica A. Delgado ◽  
Jens F. Poschet ◽  
Vojo Deretic
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Neutrophil Infiltration ◽  
Airway Epithelial Cells ◽  
Interleukin 8 ◽  
Lung Damage ◽  
Cystic Fibrosis Lung ◽  
Toll Like Receptor ◽  
Chronic Infections

ABSTRACT Pseudomonas aeruginosa is a critical colonizer of the respiratory tract in cystic fibrosis. The chronic infections with this microorganism contribute to excessive inflammation and progressive lung damage in cystic fibrosis patients. The full repertoire of Pseudomonas products that promote inflammation in the cystic fibrosis lung is not known. Here we show that P. aeruginosa DNA released from the bacterium, but not human DNA from epithelial cells or Escherichia coli DNA, displays proinflammatory properties and induces human respiratory epithelial cells to secrete interleukin-8 (IL-8), a key chemokine causing excessive neutrophil infiltration in the cystic fibrosis lung. IL-8 secretion was not due to an increase in NF-κB- or activator protein-1-dependent IL-8 promoter transcription, but instead depended on p38 and Erk mitogen-activated protein kinases. No secretion of IL-8 was observed using conventional Toll-like receptor 9 ligands (CpG oligonucleotides), although it could be demonstrated that parts of the Toll-like receptor 9-signaling pathway were functional, since class B and C CpG oligonucleotide ligands stimulated production of RANTES chemokine. The IL-8 secretion in response to P. aeruginosa DNA was decreased by treatments that inhibit acidification of intracellular organelles, using chloroquine, a pH-neutralizing compound, or bafilomycin A1, an inhibitor of vacuolar H+-ATPase. These data indicate that DNA released from P. aeruginosa during chronic infections may significantly contribute to the proinflammatory processes in cystic fibrosis. Our findings also show that treatments with drugs diminishing organellar acidification may reduce the inflammatory response in cystic fibrosis.

scholarly journals Change in Pseudomonas aeruginosa prevalence in cystic fibrosis adults over time

2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Mathew R. Crull ◽  
Kathleen J. Ramos ◽  
Ellen Caldwell ◽  
Nicole Mayer-Hamblett ◽  
Moira L. Aitken ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Over Time

scholarly journals In vitro evolution of Pseudomonas aeruginosa AA2 biofilms in the presence of cystic fibrosis lung microbiome members

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Eva Vandeplassche ◽  
Andrea Sass ◽  
Astrid Lemarcq ◽  
Ajai A. Dandekar ◽  
Tom Coenye ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Cystic Fibrosis Lung ◽  
In Vitro Evolution ◽  
Lung Microbiome

scholarly journals Pseudomonas aeruginosa Exploits Lipid A and Muropeptides Modification as a Strategy to Lower Innate Immunity during Cystic Fibrosis Lung Infection

PLoS ONE ◽  
2009 ◽  
Vol 4 (12) ◽  
pp. e8439 ◽  
Author(s):  
Cristina Cigana ◽  
Laura Curcurù ◽  
Maria Rosaria Leone ◽  
Teresa Ieranò ◽  
Nicola Ivan Lorè ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Innate Immunity ◽  
Lipid A ◽  
Lung Infection ◽  
Cystic Fibrosis Lung

scholarly journals Iron-Mediated Control of Pseudomonas aeruginosa-Staphylococcus aureus Interactions in the Cystic Fibrosis Lung

2015 ◽  
Vol 197 (14) ◽  
pp. 2250-2251 ◽  
Author(s):  
Patricia M. Barnabie ◽  
Marvin Whiteley
Keyword(s):  
Cystic Fibrosis ◽  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Patient Outcomes ◽  
Cystic Fibrosis Lung ◽  
Bacterial Survival ◽  
Content Type ◽  
Host Environment ◽  
Bacterial Interactions

Communication is an important factor for bacterial survival, growth, and persistence. Much work has examined both inter- and intraspecies interactions and their effects on virulence. Now, researchers have begun to explore the ways in which host-modulated factors can impact bacterial interactions and subsequently affect patient outcomes. In this issue, two papers discuss how the host environment alters interactions between the pathogensPseudomonas aeruginosaandStaphylococcus aureus, largely in the context of cystic fibrosis.

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