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Role of tumor necrosis factor-α and its receptors in diesel exhaust particle-induced pulmonary inflammation

Smitha Kumar UGent, Guy Joos UGent, Louis Boon, Kurt Tournoy UGent, Sharen Provoost and Tania Maes UGent (2017) SCIENTIFIC REPORTS. 7.
abstract
Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung. However, the underlying mechanisms remain to be elucidated. Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that operates by binding to tumor necrosis factor receptor 1 (TNFR1) and tumor necrosis factor receptor 2 (TNFR2). The role of TNF-alpha signaling and the importance of either TNFR1 or TNFR2 in the DEP-induced inflammatory response has not yet been elucidated. TNF-alpha knockout (KO), TNFR1 KO, TNFR2 KO, TNFR1/TNFR2 double KO (TNFR-DKO) and wild type (WT) mice were intratracheally exposed to saline or DEP. Pro-inflammatory cells and cytokines were assessed in the bronchoalveolar lavage fluid (BALF). Exposure to DEP induced a dose-dependent inflammation in the BALF in WT mice. In addition, levels of TNF-alpha and its soluble receptors were increased upon exposure to DEP. The DEP-induced inflammation in the BALF was decreased in TNF-alpha KO, TNFR-DKO and TNFR2 KO mice. In contrast, the inflammatory response in the BALF of DEP-exposed TNFR1 KO mice was largely comparable with WT controls. In conclusion, these data provide evidence for a regulatory role of TNF-alpha in DEP-induced pulmonary inflammation and identify TNFR2 as the most important receptor in mediating these inflammatory effects.
Please use this url to cite or link to this publication:
author
organization
alternative title
Role of tumor necrosis factor-alpha and its receptors in diesel exhaust particle-induced pulmonary inflammation
year
type
journalArticle (original)
publication status
published
subject
keyword
INDUCED AIRWAY HYPERRESPONSIVENESS, TO-SEVERE ASTHMA, PARTICULATE, MATTER, CONTROLLED EXPOSURE, PERIPHERAL-BLOOD, LUNG-FUNCTION, MOUSE, MODEL, RESPONSES, CELLS, MICE
journal title
SCIENTIFIC REPORTS
Sci. Rep.
volume
7
article number
11508
pages
10 pages
Web of Science type
Article
Web of Science id
000410739000006
ISSN
2045-2322
DOI
10.1038/s41598-017-11991-7
language
English
UGent publication?
yes
classification
A1
additional info
the last two authors contributed equally to this work
copyright statement
Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
id
8539389
handle
http://hdl.handle.net/1854/LU-8539389
date created
2017-11-28 09:45:02
date last changed
2017-11-29 12:49:49
@article{8539389,
  abstract     = {Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung. However, the underlying mechanisms remain to be elucidated. Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that operates by binding to tumor necrosis factor receptor 1 (TNFR1) and tumor necrosis factor receptor 2 (TNFR2). The role of TNF-alpha signaling and the importance of either TNFR1 or TNFR2 in the DEP-induced inflammatory response has not yet been elucidated. TNF-alpha knockout (KO), TNFR1 KO, TNFR2 KO, TNFR1/TNFR2 double KO (TNFR-DKO) and wild type (WT) mice were intratracheally exposed to saline or DEP. Pro-inflammatory cells and cytokines were assessed in the bronchoalveolar lavage fluid (BALF). Exposure to DEP induced a dose-dependent inflammation in the BALF in WT mice. In addition, levels of TNF-alpha and its soluble receptors were increased upon exposure to DEP. The DEP-induced inflammation in the BALF was decreased in TNF-alpha KO, TNFR-DKO and TNFR2 KO mice. In contrast, the inflammatory response in the BALF of DEP-exposed TNFR1 KO mice was largely comparable with WT controls. In conclusion, these data provide evidence for a regulatory role of TNF-alpha in DEP-induced pulmonary inflammation and identify TNFR2 as the most important receptor in mediating these inflammatory effects.},
  articleno    = {11508},
  author       = {Kumar, Smitha and Joos, Guy and Boon, Louis and Tournoy, Kurt and Provoost, Sharen and Maes, Tania},
  issn         = {2045-2322},
  journal      = {SCIENTIFIC REPORTS},
  keyword      = {INDUCED AIRWAY HYPERRESPONSIVENESS,TO-SEVERE ASTHMA,PARTICULATE,MATTER,CONTROLLED EXPOSURE,PERIPHERAL-BLOOD,LUNG-FUNCTION,MOUSE,MODEL,RESPONSES,CELLS,MICE},
  language     = {eng},
  pages        = {10},
  title        = {Role of tumor necrosis factor-\ensuremath{\alpha} and its receptors in diesel exhaust particle-induced pulmonary inflammation},
  url          = {http://dx.doi.org/10.1038/s41598-017-11991-7},
  volume       = {7},
  year         = {2017},
}

Chicago
Kumar, Smitha, Guy Joos, Louis Boon, Kurt Tournoy, Sharen Provoost, and Tania Maes. 2017. “Role of Tumor Necrosis Factor-α and Its Receptors in Diesel Exhaust Particle-induced Pulmonary Inflammation.” Scientific Reports 7.
APA
Kumar, Smitha, Joos, G., Boon, L., Tournoy, K., Provoost, S., & Maes, T. (2017). Role of tumor necrosis factor-α and its receptors in diesel exhaust particle-induced pulmonary inflammation. SCIENTIFIC REPORTS, 7.
Vancouver
1.
Kumar S, Joos G, Boon L, Tournoy K, Provoost S, Maes T. Role of tumor necrosis factor-α and its receptors in diesel exhaust particle-induced pulmonary inflammation. SCIENTIFIC REPORTS. 2017;7.
MLA
Kumar, Smitha, Guy Joos, Louis Boon, et al. “Role of Tumor Necrosis Factor-α and Its Receptors in Diesel Exhaust Particle-induced Pulmonary Inflammation.” SCIENTIFIC REPORTS 7 (2017): n. pag. Print.