Document Detail


Rhinovirus infection liberates planktonic bacteria from biofilm and increases chemokine responses in cystic fibrosis airway epithelial cells.
MedLine Citation:
PMID:  21289024     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Intermittent viral exacerbations in patients with cystic fibrosis (CF) with chronic Pseudomonas aeruginosa (PA) infection are associated with increased bacterial load. A few clinical studies suggest that rhinoviruses (RV) are associated with the majority of viral-related exacerbations in CF and require prolonged intravenous antibiotic treatment. These observations imply that acute RV infection may increase lower respiratory symptoms by increasing planktonic bacterial load. However, the underlying mechanisms are not known.
METHODS: Primary CF airway epithelial cells differentiated into mucociliary phenotype were infected with mucoid PA (MPA) followed by RV and examined for bacterial density, biofilm mass, levels of chemokines and hydrogen peroxide (H2O2). The need for dual oxidase 2, a component of NADPH oxidase, in RV-induced generation of H2O2 in CF cells was assessed using gene-specific siRNA.
RESULTS: Superinfection with RV increased chemokine responses in CF mucociliary-differentiated airway epithelial cells with pre-existing MPA infection in the form of biofilm. This was associated with the presence of planktonic bacteria at both the apical and basolateral epithelial cell surfaces. Further, RV-induced generation of H2O2 via dual oxidase 2 in CF cells was sufficient for dispersal of planktonic bacteria from the biofilm. Inhibition of NADPH oxidase reduced bacterial transmigration across mucociliary-differentiated CF cells and the interleukin-8 response in MPA- and RV-infected cells.
CONCLUSION: This study shows that acute infection with RV liberates planktonic bacteria from biofilm. Planktonic bacteria, which are more proinflammatory than their biofilm counterparts, stimulate increased chemokine responses in CF airway epithelial cells which, in turn, may contribute to the pathogenesis of CF exacerbations.
Authors:
Sangbrita S Chattoraj; Shyamala Ganesan; Andrew M Jones; Jennifer M Helm; Adam T Comstock; Rowland Bright-Thomas; John J LiPuma; Marc B Hershenson; Umadevi S Sajjan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-02-02
Journal Detail:
Title:  Thorax     Volume:  66     ISSN:  1468-3296     ISO Abbreviation:  Thorax     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-22     Completed Date:  2011-05-17     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  0417353     Medline TA:  Thorax     Country:  England    
Other Details:
Languages:  eng     Pagination:  333-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Biofilms*
Cell Differentiation
Cells, Cultured
Chemokines / biosynthesis*
Cystic Fibrosis / immunology,  microbiology*,  virology
Epithelial Cells / immunology,  microbiology,  ultrastructure,  virology
Humans
Hydrogen Peroxide / metabolism
Interleukin-8 / biosynthesis
Microscopy, Electron, Scanning
Picornaviridae Infections / complications*
Pseudomonas Infections / complications
Pseudomonas aeruginosa / physiology*
Respiratory Mucosa / immunology,  microbiology,  ultrastructure,  virology
Rhinovirus / isolation & purification
Superinfection / complications
Viral Load
Grant Support
ID/Acronym/Agency:
HL081420/HL/NHLBI NIH HHS; HL082550/HL/NHLBI NIH HHS; HL0897720/HL/NHLBI NIH HHS; R01 HL081420/HL/NHLBI NIH HHS; R01 HL081420-01A1/HL/NHLBI NIH HHS; R01 HL081420-07/HL/NHLBI NIH HHS; R01 HL082550/HL/NHLBI NIH HHS; R01 HL082550-01/HL/NHLBI NIH HHS; R21 HL089772/HL/NHLBI NIH HHS; R21 HL089772-01A1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Chemokines; 0/Interleukin-8; BBX060AN9V/Hydrogen Peroxide
Comments/Corrections

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