TNF receptor associated factor 5 controls oncostatin M-mediated lung inflammation

Tomoaki Machiyama, Takanori So, Yuko Okuyama, Shuhei Kobayashi, Hai The Phung, Atsuko Asao, Hideo Harigae, Naoto Ishii

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Oncostatin M (OSM) is involved in pathogenesis of several human inflammatory diseases including lung inflammation and fibrosis. Although accumulating evidence indicates that OSM mediates lung inflammation, the precise mechanism for OSM on lung inflammation still remains unclear. In this study, we found that OSM receptor was abundantly expressed on endothelial and stromal/fibroblast cells in the lung of mice. In vitro stimulation with OSM upregulated vascular cell adhesion molecule-1 (VCAM-1), which promotes eosinophil infiltration in the lung tissues, on freshly-isolated lung stromal/fibroblast cells from wild-type mice. However, these cells from TNF receptor associated factor 5 (TRAF5)-deficient mice failed to show the increase in VCAM-1 expression after OSM stimulation. Furthermore, Traf5−/− mice showed markedly attenuated lung inflammation in terms of eosinophil infiltration upon intranasal administration with OSM as compared to wild-type mice. These results indicate that TRAF5 is crucially involved in OSM-mediated lung inflammation probably by inducing lung stromal/fibroblast cell activation.

Original languageEnglish
Pages (from-to)544-550
Number of pages7
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2018 May 15


  • Lung endothelial cell
  • Lung stromal/fibroblast cells
  • Oncostatin M
  • Traf5
  • VCAM-1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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