Advanced search
1 file | 535.49 KB Add to list

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) , Guy Joos (UGent) , et al.
Author
Organization
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.
Keywords
RHINITIS, SINUSITIS, EMPHYSEMA, OBSTRUCTIVE PULMONARY-DISEASE, COPD, CELLS, MICE, MECHANISMS, ASTHMA

Downloads

  • W Huvenne.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 535.49 KB

Citation

Please use this url to cite or link to this publication:

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.
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).
Chicago author-date
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).
Chicago author-date (all authors)
Huvenne, Wouter, Claudina Perez Novo, Lara Derycke, Natalie De Ruyck, Olga Krysko, Tania Maes, Nele Pauwels, Lander Robays, Ken Bracke, Guy Joos, Guy Brusselle, and Claus Bachert. 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).
IEEE
[1]
W. Huvenne et al., “Different regulation of cigarette smoke induced inflammation in upper versus lower airways,” RESPIRATORY RESEARCH, vol. 11, no. 1, 2010.
@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},
  keywords     = {RHINITIS,SINUSITIS,EMPHYSEMA,OBSTRUCTIVE PULMONARY-DISEASE,COPD,CELLS,MICE,MECHANISMS,ASTHMA},
  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},
}

Altmetric
View in Altmetric
Web of Science
Times cited: