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Impact of chronic pulmonary infection with Pseudomonas aeruginosa on transfection mediated by viral and nonviral vectors

Joanna Rejman UGent, Ida De Fino, Moira Paroni, Alessandra Bragonzi, Jo Demeester UGent, Stefaan De Smedt UGent and Massimo Conese (2010) HUMAN GENE THERAPY. 21(3). p.351-356
abstract
Pseudomonas aeruginosa plays a crucial role in the lung pathology of cystic fibrosis (CF). We showed that acute infection with P. aeruginosa has a substantial impact on gene transfer into lung epithelial cells mediated by polyplexes. As an extension of those studies we report here on the effect of chronic pulmonary infection with P. aeruginosa on transfection of lung epithelial cells by viral and nonviral vectors. As an in vivo model of the persistent chronic infection in patients with CF we used C57BL/6 mice intratracheally infected with P. aeruginosa encapsulated in agar beads. Two weeks after infection the presence of viable bacteria in the lungs was confirmed, mostly in the bronchial lumen. In lung tissue sections stained with hematoxylin and eosin, extensive inflammatory infiltrations were found. At that time point the mice received an intratracheal dose of luciferase gene complexed with either Lipofectamine (Lf), a GL67 lipid mixture (GL67), or polyethylenimine (PEI) or with lentivirus (LV) as a carrier system. Luciferase activity was determined by a luminescence assay in supernatants of lung homogenates. The transfection level induced by PEI/DNA polyplexes complexed with serum albumin was decreased in infected mice. Lf-mediated transfection was almost completely blocked in infected mice. Transfection levels in mice treated with LV or plain PEI/DNA polyplexes were unchanged in infected animals as compared with control mice. The only carrier that displayed a clearly increased transfection level in infected mice was the GL67 lipid mixture, which is tentatively ascribed to the presence of polyethylene glycol in this carrier.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CFTR, INFLAMMATION, MODULATION, LUNGS, MICE, ADENOVIRUS, IN-VIVO, CYSTIC-FIBROSIS, AIRWAY EPITHELIAL-CELLS, GENE-TRANSFER
journal title
HUMAN GENE THERAPY
Hum. Gene Ther.
volume
21
issue
3
pages
351 - 356
Web of Science type
Article
Web of Science id
000275680700009
JCR category
BIOTECHNOLOGY & APPLIED MICROBIOLOGY
JCR impact factor
4.829 (2010)
JCR rank
19/158 (2010)
JCR quartile
1 (2010)
ISSN
1043-0342
DOI
10.1089/hum.2009.085
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1899508
handle
http://hdl.handle.net/1854/LU-1899508
date created
2011-09-09 11:05:56
date last changed
2016-12-19 15:46:42
@article{1899508,
  abstract     = {Pseudomonas aeruginosa plays a crucial role in the lung pathology of cystic fibrosis (CF). We showed that acute infection with P. aeruginosa has a substantial impact on gene transfer into lung epithelial cells mediated by polyplexes. As an extension of those studies we report here on the effect of chronic pulmonary infection with P. aeruginosa on transfection of lung epithelial cells by viral and nonviral vectors. As an in vivo model of the persistent chronic infection in patients with CF we used C57BL/6 mice intratracheally infected with P. aeruginosa encapsulated in agar beads. Two weeks after infection the presence of viable bacteria in the lungs was confirmed, mostly in the bronchial lumen. In lung tissue sections stained with hematoxylin and eosin, extensive inflammatory infiltrations were found. At that time point the mice received an intratracheal dose of luciferase gene complexed with either Lipofectamine (Lf), a GL67 lipid mixture (GL67), or polyethylenimine (PEI) or with lentivirus (LV) as a carrier system. Luciferase activity was determined by a luminescence assay in supernatants of lung homogenates. The transfection level induced by PEI/DNA polyplexes complexed with serum albumin was decreased in infected mice. Lf-mediated transfection was almost completely blocked in infected mice. Transfection levels in mice treated with LV or plain PEI/DNA polyplexes were unchanged in infected animals as compared with control mice. The only carrier that displayed a clearly increased transfection level in infected mice was the GL67 lipid mixture, which is tentatively ascribed to the presence of polyethylene glycol in this carrier.},
  author       = {Rejman, Joanna and De Fino, Ida and Paroni, Moira and Bragonzi, Alessandra and Demeester, Jo and De Smedt, Stefaan and Conese, Massimo},
  issn         = {1043-0342},
  journal      = {HUMAN GENE THERAPY},
  keyword      = {CFTR,INFLAMMATION,MODULATION,LUNGS,MICE,ADENOVIRUS,IN-VIVO,CYSTIC-FIBROSIS,AIRWAY EPITHELIAL-CELLS,GENE-TRANSFER},
  language     = {eng},
  number       = {3},
  pages        = {351--356},
  title        = {Impact of chronic pulmonary infection with Pseudomonas aeruginosa on transfection mediated by viral and nonviral vectors},
  url          = {http://dx.doi.org/10.1089/hum.2009.085},
  volume       = {21},
  year         = {2010},
}

Chicago
Rejman, Joanna, Ida De Fino, Moira Paroni, Alessandra Bragonzi, Jo Demeester, Stefaan De Smedt, and Massimo Conese. 2010. “Impact of Chronic Pulmonary Infection with Pseudomonas Aeruginosa on Transfection Mediated by Viral and Nonviral Vectors.” Human Gene Therapy 21 (3): 351–356.
APA
Rejman, J., De Fino, I., Paroni, M., Bragonzi, A., Demeester, J., De Smedt, S., & Conese, M. (2010). Impact of chronic pulmonary infection with Pseudomonas aeruginosa on transfection mediated by viral and nonviral vectors. HUMAN GENE THERAPY, 21(3), 351–356.
Vancouver
1.
Rejman J, De Fino I, Paroni M, Bragonzi A, Demeester J, De Smedt S, et al. Impact of chronic pulmonary infection with Pseudomonas aeruginosa on transfection mediated by viral and nonviral vectors. HUMAN GENE THERAPY. 2010;21(3):351–6.
MLA
Rejman, Joanna, Ida De Fino, Moira Paroni, et al. “Impact of Chronic Pulmonary Infection with Pseudomonas Aeruginosa on Transfection Mediated by Viral and Nonviral Vectors.” HUMAN GENE THERAPY 21.3 (2010): 351–356. Print.