T.S. and K.F. contributed equally to this work.
Cell type-dependent effects of corticosteroid on periostin production by primary human tissue cells
Article first published online: 10 OCT 2013
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 68, Issue 11, pages 1467–1470, November 2013
How to Cite
Cell type-dependent effects of corticosteroid on periostin production by primary human tissue cells. Allergy 2013; 68: 1467–1470., , , , , .
Edited by: Michael Wechsler
- Issue published online: 30 OCT 2013
- Article first published online: 10 OCT 2013
- Manuscript Accepted: 20 JUL 2013
- National Institute of Biomedical Innovation. Grant Number: ID10-43
- Grant of National Center for Child Health and Development. Grant Number: 23A-5
- JSPS KAKENHI. Grant Number: 23591666
- microvascular endothelial cells;
Overproduction of periostin, an IL-13-inducible matricellular protein, despite corticosteroid treatment is thought to be involved in the chronicity of allergic inflammation seen in corticosteroid-refractory tissue fibrosis. Therefore, we hypothesized that some tissue cells must produce periostin in a corticosteroid-insensitive manner. Here, we show that IL-4 and IL-13 each induced comparable levels of periostin production by primary normal human fibroblasts and microvascular endothelial cells derived from lung and skin. Dexamethasone, a corticosteroid, completely inhibited IL-4/13-induced, but did not affect TGF-β-induced, periostin production by fibroblasts. In contrast, dexamethasone synergistically enhanced IL-4/13-induced periostin production by microvascular endothelial cells. TGF-β did not induce periostin production by microvascular endothelial cells. Our novel findings suggest that IL-4/13-induced microvascular endothelium-derived and/or TGF-β-induced fibroblast-derived periostin might play a pivotal role in corticosteroid-refractory tissue fibrosis, leading to chronic allergic inflammation in the lung and/or skin.