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Different regulation of cigarette smoke induced inflammation in upper versus lower airways

WOUTER HUVENNE UGent, Claudina Perez Novo UGent, LARA DERYCKE UGent, Natalie De Ruyck UGent, Olga Krysko UGent, Tania Maes UGent, Nele Pauwels UGent, Lander Robays UGent, Ken Bracke UGent and Guy Joos UGent, et al. (2010) RESPIRATORY RESEARCH. 11(1).
abstract
Background: Cigarette smoke (CS) is known to initiate a cascade of mediator release and accumulation of immune and inflammatory cells in the lower airways. We investigated and compared the effects of CS on upper and lower airways, in a mouse model of subacute and chronic CS exposure. Methods: C57BL/6 mice were whole-body exposed to mainstream CS or air, for 2, 4 and 24 weeks. Bronchoalveolar lavage fluid (BAL) was obtained and tissue cryosections from nasal turbinates were stained for neutrophils and T cells. Furthermore, we evaluated GCP-2, KC, MCP-1, MIP-3 alpha, RORc, IL-17, FoxP3, and TGF-beta 1 in nasal turbinates and lungs by RT-PCR. Results: In both upper and lower airways, subacute CS-exposure induced the expression of GCP-2, MCP-1, MIP-3a and resulted in a neutrophilic influx. However, after chronic CS-exposure, there was a significant downregulation of inflammation in the upper airways, while on the contrary, lower airway inflammation remained present. Whereas nasal FoxP3 mRNA levels already increased after 2 weeks, lung FoxP3 mRNA increased only after 4 weeks, suggesting that mechanisms to suppress inflammation occur earlier and are more efficient in nose than in lungs. Conclusions: Altogether, these data demonstrate that CS induced inflammation may be differently regulated in the upper versus lower airways in mice. Furthermore, these data may help to identify new therapeutic targets in this disease model.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CELLS, COPD, OBSTRUCTIVE PULMONARY-DISEASE, EMPHYSEMA, RHINITIS, SINUSITIS, ASTHMA, MICE, MECHANISMS
journal title
RESPIRATORY RESEARCH
Respir. Res.
volume
11
issue
1
article_number
100
pages
9 pages
Web of Science type
Article
Web of Science id
000282550700001
JCR category
RESPIRATORY SYSTEM
JCR impact factor
2.859 (2010)
JCR rank
14/45 (2010)
JCR quartile
2 (2010)
ISSN
1465-9921
DOI
10.1186/1465-9921-11-100
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1031430
handle
http://hdl.handle.net/1854/LU-1031430
date created
2010-09-01 14:45:26
date last changed
2011-06-01 10:29:02
@article{1031430,
  abstract     = {Background: Cigarette smoke (CS) is known to initiate a cascade of mediator release and accumulation of immune and inflammatory cells in the lower airways. We investigated and compared the effects of CS on upper and lower airways, in a mouse model of subacute and chronic CS exposure. Methods: C57BL/6 mice were whole-body exposed to mainstream CS or air, for 2, 4 and 24 weeks. Bronchoalveolar lavage fluid (BAL) was obtained and tissue cryosections from nasal turbinates were stained for neutrophils and T cells. Furthermore, we evaluated GCP-2, KC, MCP-1, MIP-3 alpha, RORc, IL-17, FoxP3, and TGF-beta 1 in nasal turbinates and lungs by RT-PCR. Results: In both upper and lower airways, subacute CS-exposure induced the expression of GCP-2, MCP-1, MIP-3a and resulted in a neutrophilic influx. However, after chronic CS-exposure, there was a significant downregulation of inflammation in the upper airways, while on the contrary, lower airway inflammation remained present. Whereas nasal FoxP3 mRNA levels already increased after 2 weeks, lung FoxP3 mRNA increased only after 4 weeks, suggesting that mechanisms to suppress inflammation occur earlier and are more efficient in nose than in lungs. Conclusions: Altogether, these data demonstrate that CS induced inflammation may be differently regulated in the upper versus lower airways in mice. Furthermore, these data may help to identify new therapeutic targets in this disease model.},
  articleno    = {100},
  author       = {HUVENNE, WOUTER and Perez Novo, Claudina and DERYCKE, LARA and De Ruyck, Natalie and Krysko, Olga and Maes, Tania and Pauwels, Nele and Robays, Lander and Bracke, Ken and Joos, Guy and Brusselle, Guy and Bachert, Claus},
  issn         = {1465-9921},
  journal      = {RESPIRATORY RESEARCH},
  keyword      = {CELLS,COPD,OBSTRUCTIVE PULMONARY-DISEASE,EMPHYSEMA,RHINITIS,SINUSITIS,ASTHMA,MICE,MECHANISMS},
  language     = {eng},
  number       = {1},
  pages        = {9},
  title        = {Different regulation of cigarette smoke induced inflammation in upper versus lower airways},
  url          = {http://dx.doi.org/10.1186/1465-9921-11-100},
  volume       = {11},
  year         = {2010},
}

Chicago
HUVENNE, WOUTER, Claudina Perez Novo, LARA DERYCKE, Natalie De Ruyck, Olga Krysko, Tania Maes, Nele Pauwels, et al. 2010. “Different Regulation of Cigarette Smoke Induced Inflammation in Upper Versus Lower Airways.” Respiratory Research 11 (1).
APA
HUVENNE, W., Perez Novo, C., DERYCKE, L., De Ruyck, N., Krysko, O., Maes, T., Pauwels, N., et al. (2010). Different regulation of cigarette smoke induced inflammation in upper versus lower airways. RESPIRATORY RESEARCH, 11(1).
Vancouver
1.
HUVENNE W, Perez Novo C, DERYCKE L, De Ruyck N, Krysko O, Maes T, et al. Different regulation of cigarette smoke induced inflammation in upper versus lower airways. RESPIRATORY RESEARCH. 2010;11(1).
MLA
HUVENNE, WOUTER, Claudina Perez Novo, LARA DERYCKE, et al. “Different Regulation of Cigarette Smoke Induced Inflammation in Upper Versus Lower Airways.” RESPIRATORY RESEARCH 11.1 (2010): n. pag. Print.