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    Effects of CFTR, interleukin-10, and Pseudomonas aeruginosa on gene expression profiles in a CF bronchial epithelial cell Line

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    Authors
    Virella-Lowell, Isabel
    Herlihy, John-David
    Liu, Barry
    Lopez, Cecilia
    Cruz, Pedro
    Mueller, Christian
    Baker, Henry V.
    Flotte, Terence R.
    UMass Chan Affiliations
    Gene Therapy Center
    Department of Pediatrics
    Document Type
    Journal Article
    Publication Date
    2004-09-01
    Keywords
    Cystic Fibrosis
    Cystic Fibrosis Transmembrane Conductance Regulator
    Gene Expression Profiling
    Interleukin-10
    Pseudomonas aeruginosa
    Allergy and Immunology
    Pediatrics
    Respiratory Tract Diseases
    
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    Link to Full Text
    http://dx.doi.org/10.1016/j.ymthe.2004.06.215
    Abstract
    Mutations in CFTR lead to a complex phenotype that includes increased susceptibility to Pseudomonas infections, a functional deficiency of IL-10, and an exaggerated proinflammatory cytokine response. We examined the effects of CFTR gene correction on the gene expression profile of a CF bronchial epithelial cell line (IB3-1) and determined which CF-related gene expression changes could be reversed by IL-10 expression. We performed microarray experiments to monitor the gene expression profile of three cell lines over a time course of exposure to Pseudomonas. At baseline, we identified 843 genes with statistically different levels of expression in CFTR-corrected (S9) cells compared to the IB3-1 line or the IL-10-expressing line. K-means clustering and functional group analysis revealed a primary up-regulation of ubiquitination enzymes and TNF pathway components and a primary down-regulation of protease inhibitors and protein glycosylation enzymes in CF. Key gene expression changes were confirmed by real-time RT-PCR. Massive reprogramming of gene expression occurred 3 h after Pseudomonas exposure. Changes specific to CF included exaggerated activation of cytokines, blunted activation of anti-proteases, and repression of protein glycosylation enzymes. In conclusion, the CFTR genotype changes the expression of multiple genes at baseline and in response to bacterial challenge, and only a subset of these changes is secondary to IL-10 deficiency.
    Source

    Mol Ther. 2004 Sep;10(3):562-73.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/43852
    PubMed ID
    15336656
    Notes

    Christian Mueller is cited on this publication as Chris Muller. At the time of publication, Christian Mueller and Terence Flotte were not yet affiliated with the University of Massachusetts Medical School.

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