Eosinophil Cationic Protein Stimulates TGF-β1 Release by Human Lung Fibroblasts In Vitro
2007 (English)In: Inflammation, ISSN 0360-3997, E-ISSN 1573-2576, Vol. 30, no 5, 153-160 p.Article in journal (Refereed) Published
Eosinophilic inflammation and airway remodeling are features of asthma. Eosinophil cationic protein ( ECP) is released by activated eosinophils and transforming growth factor ( TGF)beta(1) has major functions in the fibrotic process. We therefore hypothesized that ECP stimulates TGF-beta(1) release by human lung fibroblasts. Fibroblasts in monolayer displayed a constitutive release of TGF-beta(1), which increased in presence of ECP ( 436 +/- 60 vs. 365 +/- 48 pg/ ml at 48 h; P< 0.01). mRNA expression of TGF-beta(1) was almost twofold in ECP- stimulated fibroblasts. ECP in threedimensional cultures stimulated both TGF-beta(1) release ( 180 +/- 61 vs. 137 +/- 54 pg/ ml; P< 0.01) and fibroblast- mediated collagen gel contraction ( 28 vs. 39% of initial gel area at 48 h; P< 0.001). ECP stimulates TGF-beta(1) release by human lung fibroblasts, suggesting a potential mechanism for eosinophils in the fibrotic response. This may be an important mechanism by which ECP promotes remodeling of extra cellular matrix leading to airway fibrosis in asthmatics.
Place, publisher, year, edition, pages
2007. Vol. 30, no 5, 153-160 p.
Cell Proliferation, Cells; Cultured, Coculture Techniques, Collagen/metabolism, Eosinophil Cationic Protein/*metabolism, Eosinophils/*metabolism, Fibroblasts/*metabolism, Gels, Humans, Lung/embryology/*metabolism, Pulmonary Fibrosis/metabolism, RNA; Messenger/metabolism, Time Factors, Transforming Growth Factor beta1/genetics/*metabolism
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-13872DOI: 10.1007/s10753-007-9032-4ISI: 000250118500004PubMedID: 17587163OAI: oai:DiVA.org:uu-13872DiVA: diva2:41642