期刊
ALLERGY
卷 68, 期 11, 页码 1467-1470出版社
WILEY-BLACKWELL
DOI: 10.1111/all.12240
关键词
corticosteroid; fibroblasts; IL-13; microvascular endothelial cells; periostin
资金
- National Institute of Biomedical Innovation [ID10-43]
- National Center for Child Health and Development [23A-5]
- JSPS KAKENHI [23591666]
- Grants-in-Aid for Scientific Research [23591666] Funding Source: KAKEN
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--induced, periostin production by fibroblasts. In contrast, dexamethasone synergistically enhanced IL-4/13-induced periostin production by microvascular endothelial cells. TGF- did not induce periostin production by microvascular endothelial cells. Our novel findings suggest that IL-4/13-induced microvascular endothelium-derived and/or TGF--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.
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