Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 118, Issue 1, Pages 98-104Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2006.02.046
Keywords
bronchial asthma; IL-4; IL-13; periostin; TGF-beta; subepithelial fibrosis; basement membrane; extracellular matrix protein; fibronectin; tenascin-C
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Funding
- Medical Research Council [MC_U105178805] Funding Source: researchfish
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: Medline
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Background: Subepithelial fibrosis is a cardinal feature of bronchial asthma. Collagen I, III, and V; fibronectin; and tenascin-C are deposited in the lamina reticularis. Extensive evidence supports the pivotal role of IL-4 and IL-13 in subepithelial fibrosis; however, the precise mechanism remains unclear. We have previously identified the POSTN gene encoding periostin as an IL-4/IL-13-inducible gene in bronchial epithelial cells. Periostin is thought to be an adhesion molecule because it possesses 4 fasciclin I domains. Objective: We explore the possibility that periostin is involved in subepithelial fibrosis in bronchial asthma. Methods: We analyzed induction of periostin in lung fibroblasts by IL-4 or IL-13. We next analyzed expression of periostin in patients with asthma and in ovalbumin-sensitized and ovalbumin-inhaled mice. Furthermore, we examined the binding ability of periostin to other extracellular matrix proteins. Results: Both IL-4 and IL-13 induced secretion of periostin in lung fibroblasts independently of TGF-beta. Periostin colocalized with other extracellular matrix proteins involved in subepithelial fibrosis in both asthma patients and ovalbumin-sensitized and ovalbumin-inhaled wild-type mice, but not in either IL-4 or IL-13 knockout mice. Periostin had an ability to bind to fibronectin, tenascin-C, collagen V, and periostin itself. C onclusion: Periostin secreted by lung fibroblasts in response to IL-4 and/or IL-13 is a novel component of subepithelial fibrosis in bronchial asthma. Periostin may contribute to this process by binding to other extracellular matrix proteins. Clinical implications: Periostin induced by IL-4/IL-13 shows promise in inhibiting subepithelial fibrosis in bronchial asthma.
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