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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 (UGent) and Tania Maes (UGent)
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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.
Keywords
INDUCED AIRWAY HYPERRESPONSIVENESS, TO-SEVERE ASTHMA, PARTICULATE, MATTER, CONTROLLED EXPOSURE, PERIPHERAL-BLOOD, LUNG-FUNCTION, MOUSE, MODEL, RESPONSES, CELLS, MICE

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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.
@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},
}

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