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The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice

Liesbeth Allais, Smitha Kumar UGent, Karlijn Debusschere UGent, STEPHANIE VERSCHUERE, Tania Maes UGent, Rebecca De Smet, Griet Conickx UGent, Martine De Vos UGent, Debby Laukens UGent, Guy Joos UGent, et al. (2015) PLOS ONE. 10(11).
abstract
The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure.
Please use this url to cite or link to this publication:
author
organization
alternative title
The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNF Delta ARE mice
year
type
journalArticle (original)
publication status
published
subject
keyword
SPONDYLOARTHRITIS, IMMUNE-RESPONSE, INDUCED PULMONARY INFLAMMATION, CYTOKINE MESSENGER-RNA, TUMOR-NECROSIS-FACTOR, BOWEL-DISEASE, FACTOR-ALPHA, EXTRAINTESTINAL MANIFESTATIONS, RHEUMATOID-ARTHRITIS, TOBACCO-SMOKE
journal title
PLOS ONE
PLoS One
volume
10
issue
11
article number
e0141570
pages
16 pages
Web of Science type
Article
Web of Science id
000364029800011
JCR category
MULTIDISCIPLINARY SCIENCES
JCR impact factor
3.057 (2015)
JCR rank
11/63 (2015)
JCR quartile
1 (2015)
ISSN
1932-6203
DOI
10.1371/journal.pone.0141570
language
English
UGent publication?
yes
classification
A1
additional info
the first two authors contributed equally to this work the last two authors contributed equally to the study supervision
copyright statement
I have retained and own the full copyright for this publication
id
7001772
handle
http://hdl.handle.net/1854/LU-7001772
date created
2015-12-04 12:42:49
date last changed
2016-12-21 15:42:00
@article{7001772,
  abstract     = {The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure.},
  articleno    = {e0141570},
  author       = {Allais, Liesbeth and Kumar, Smitha and Debusschere, Karlijn and VERSCHUERE, STEPHANIE and Maes, Tania and De Smet, Rebecca and Conickx, Griet and De Vos, Martine and Laukens, Debby and Joos, Guy and Brusselle, Guy and Elewaut, Dirk and Cuvelier, Claude and Bracke, Ken},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keyword      = {SPONDYLOARTHRITIS,IMMUNE-RESPONSE,INDUCED PULMONARY INFLAMMATION,CYTOKINE MESSENGER-RNA,TUMOR-NECROSIS-FACTOR,BOWEL-DISEASE,FACTOR-ALPHA,EXTRAINTESTINAL MANIFESTATIONS,RHEUMATOID-ARTHRITIS,TOBACCO-SMOKE},
  language     = {eng},
  number       = {11},
  pages        = {16},
  title        = {The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNF\ensuremath{\Delta}ARE mice},
  url          = {http://dx.doi.org/10.1371/journal.pone.0141570},
  volume       = {10},
  year         = {2015},
}

Chicago
Allais, Liesbeth, Smitha Kumar, Karlijn Debusschere, STEPHANIE VERSCHUERE, Tania Maes, Rebecca De Smet, Griet Conickx, et al. 2015. “The Effect of Cigarette Smoke Exposure on the Development of Inflammation in Lungs, Gut and Joints of TNFΔARE Mice.” Plos One 10 (11).
APA
Allais, L., Kumar, S., Debusschere, K., VERSCHUERE, S., Maes, T., De Smet, R., Conickx, G., et al. (2015). The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice. PLOS ONE, 10(11).
Vancouver
1.
Allais L, Kumar S, Debusschere K, VERSCHUERE S, Maes T, De Smet R, et al. The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice. PLOS ONE. 2015;10(11).
MLA
Allais, Liesbeth, Smitha Kumar, Karlijn Debusschere, et al. “The Effect of Cigarette Smoke Exposure on the Development of Inflammation in Lungs, Gut and Joints of TNFΔARE Mice.” PLOS ONE 10.11 (2015): n. pag. Print.