scholarly journals Lactoferrin Decreases Inflammatory Response by Cystic Fibrosis Bronchial Cells Invaded with Burkholderia Cenocepacia Iron-Modulated Biofilm

2011 ◽  
Vol 24 (4) ◽  
pp. 1057-1068 ◽  
Author(s):  
P. Valenti ◽  
A. Catizone ◽  
F. Pantanella ◽  
A. Frioni ◽  
T. Natalizi ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Inflammatory Response ◽  
Burkholderia Cenocepacia ◽  
Bronchial Cells

scholarly journals MPB-07 Reduces the Inflammatory Response toPseudomonas aeruginosain Cystic Fibrosis Bronchial Cells

2007 ◽  
Vol 36 (5) ◽  
pp. 615-624 ◽  
Author(s):  
Maria Cristina Dechecchi ◽  
Elena Nicolis ◽  
Valentino Bezzerri ◽  
Antonio Vella ◽  
Marco Colombatti ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Inflammatory Response ◽  
Bronchial Cells

scholarly journals The isoprenoid end product N6-isopentenyladenosine reduces inflammatory response through the inhibition of the NFκB and STAT3 pathways in cystic fibrosis cells

2017 ◽  
Vol 67 (4) ◽  
pp. 315-326 ◽  
Author(s):  
Antonietta Santoro ◽  
Elena Ciaglia ◽  
Vanessa Nicolin ◽  
Alessandra Pescatore ◽  
Lucia Prota ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Inflammatory Response

scholarly journals Vx-809/Vx-770 treatment reduces inflammatory response to Pseudomonas aeruginosa in primary differentiated cystic fibrosis bronchial epithelial cells

2018 ◽  
Vol 314 (4) ◽  
pp. L635-L641 ◽  
Author(s):  
Manon Ruffin ◽  
Lucie Roussel ◽  
Émilie Maillé ◽  
Simon Rousseau ◽  
Emmanuelle Brochiero
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Inflammatory Response ◽  
Respiratory Infections ◽  
Bronchial Epithelial Cell ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Bronchial Epithelial ◽  
Primary Bronchial Epithelial Cell ◽  
Beneficial Impact

Cystic fibrosis patients exhibit chronic Pseudomonas aeruginosa respiratory infections and sustained proinflammatory state favoring lung tissue damage and remodeling, ultimately leading to respiratory failure. Loss of cystic fibrosis transmembrane conductance regulator (CFTR) function is associated with MAPK hyperactivation and increased cytokines expression, such as interleukin-8 [chemoattractant chemokine (C-X-C motif) ligand 8 (CXCL8)]. Recently, new therapeutic strategies directly targeting the basic CFTR defect have been developed, and ORKAMBI (Vx-809/Vx-770 combination) is the only Food and Drug Administration-approved treatment for CF patients homozygous for the F508del mutation. Here we aimed to determine the effect of the Vx-809/Vx-770 combination on the induction of the inflammatory response by fully differentiated primary bronchial epithelial cell cultures from CF patients carrying F508del mutations, following exposure to P. aeruginosa exoproducts. Our data unveiled that CFTR functional rescue with Vx-809/Vx-770 drastically reduces CXCL8 (as well as CXCL1 and CXCL2) transcripts and p38 MAPK phosphorylation in response to P. aeruginosa exposure through a CFTR-dependent mechanism. These results suggest that ORKAMBI has anti-inflammatory properties that could decrease lung inflammation and contribute to the observed beneficial impact of this treatment in CF patients.

scholarly journals Effect of Aspergillus fumigatus and Candida albicans on pro-inflammatory response in cystic fibrosis epithelium

2011 ◽  
Vol 10 (6) ◽  
pp. 401-406 ◽  
Author(s):  
James A. Reihill ◽  
John E. Moore ◽  
J. Stuart Elborn ◽  
Madeleine Ennis
Keyword(s):  
Cystic Fibrosis ◽  
Candida Albicans ◽  
Inflammatory Response ◽  
Aspergillus Fumigatus

scholarly journals Improved Electrotransformation and Decreased Antibiotic Resistance of the Cystic Fibrosis Pathogen Burkholderia cenocepacia Strain J2315

2009 ◽  
Vol 76 (4) ◽  
pp. 1095-1102 ◽  
Author(s):  
Nelly Dubarry ◽  
Wenli Du ◽  
David Lane ◽  
Franck Pasta
Keyword(s):  
Cystic Fibrosis ◽  
Antibiotic Resistance ◽  
Resistance Genes ◽  
Efflux Pump ◽  
Antibiotic Resistance Genes ◽  
Burkholderia Cenocepacia ◽  
The Poor ◽  
High Level

ABSTRACT The bacterium Burkholderia cenocepacia is pathogenic for sufferers from cystic fibrosis (CF) and certain immunocompromised conditions. The B. cenocepacia strain most frequently isolated from CF patients, and which serves as the reference for CF epidemiology, is J2315. The J2315 genome is split into three chromosomes and one plasmid. The strain was sequenced several years ago, and its annotation has been released recently. This information should allow genetic experimentation with J2315, but two major impediments appear: the poor potential of J2315 to act as a recipient in transformation and conjugation and the high level of resistance it mounts to nearly all antibiotics. Here, we describe modifications to the standard electroporation procedure that allow routine transformation of J2315 by DNA. In addition, we show that deletion of an efflux pump gene and addition of spermine to the medium enhance the sensitivity of J2315 to certain commonly used antibiotics and so allow a wider range of antibiotic resistance genes to be used for selection.

Albumin Metabolism in Cystic Fibrosis

PEDIATRICS ◽  
1969 ◽  
Vol 44 (2) ◽  
pp. 305-306
Author(s):  
A. Myron Johnson
Keyword(s):  
Cystic Fibrosis ◽  
Inflammatory Response ◽  
Blood Volume ◽  
Acute Inflammatory Response ◽  
Albumin Synthesis ◽  
Compensatory Response ◽  
Normal Albumin

It appears that Dr. Strober and I disagree on the implications of the word "cause" (Pediatrics, 44:144, 1969). The paper in question did not even consider the possibility that some other factor(s) could result in increased blood volume and decreased albumin synthesis concurrently. One possible third factor is the acute inflammatory response. If such be the case, even normal albumin synthesis may represent a compensatory response to the hypervolemia. The arguments in Dr. Strober's reply are based, in part, on the speculation that the liver is incapable of producing albumin at a rate much above the normal, resting rate.

scholarly journals In Vitro Activity of a Novel Glycopolymer against Biofilms of Burkholderia cepacia Complex Cystic Fibrosis Clinical Isolates

2019 ◽  
Vol 63 (6) ◽  
Author(s):  
Vidya P. Narayanaswamy ◽  
Andrew P. Duncan ◽  
John J. LiPuma ◽  
William P. Wiesmann ◽  
Shenda M. Baker ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Burkholderia Cepacia ◽  
Laser Scanning Microscopy ◽  
Burkholderia Cenocepacia ◽  
Burkholderia Cepacia Complex ◽  
Confocal Laser ◽  
Content Type ◽  
Biofilm Removal ◽  
Increased Risk

ABSTRACT Burkholderia cepacia complex (Bcc) lung infections in cystic fibrosis (CF) patients are often associated with a steady decline in lung function and death. The formation of biofilms and inherent multidrug resistance are virulence factors associated with Bcc infection and contribute to increased risk of mortality in CF patients. New therapeutic strategies targeting bacterial biofilms are anticipated to enhance antibiotic penetration and facilitate resolution of infection. Poly (acetyl, arginyl) glucosamine (PAAG) is a cationic glycopolymer therapeutic being developed to directly target biofilm integrity. In this study, 13 isolates from 7 species were examined, including Burkholderia multivorans, Burkholderia cenocepacia, Burkholderia gladioli, Burkholderia dolosa, Burkholderia vietnamiensis, and B. cepacia. These isolates were selected for their resistance to standard clinical antibiotics and their ability to form biofilms in vitro. Biofilm biomass was quantitated using static tissue culture plate (TCP) biofilm methods and a minimum biofilm eradication concentration (MBEC) assay. Confocal laser scanning microscopy (CLSM) visualized biofilm removal by PAAG during treatment. Both TCP and MBEC methods demonstrated a significant dose-dependent relationship with regard to biofilm removal by 50 to 200 μg/ml PAAG following a 1-h treatment (P < 0.01). A significant reduction in biofilm thickness was observed following a 10-min treatment of Bcc biofilms with PAAG compared to that with vehicle control (P < 0.001) in TCP, MBEC, and CLSM analyses. PAAG also rapidly permeabilizes bacteria within the first 10 min of treatment. Glycopolymers, such as PAAG, are a new class of large-molecule therapeutics that support the treatment of recalcitrant Bcc biofilm.

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