The persistent high number of eosinophils and ECP in the lungs of allergic asthmatics has led to the suggestion of their participation in the development of chronic lung tissue remodelling. Remodelling has also been found in the esophagus of patients with eosinophil esophagitis [103] and sECP has been found elevated in one case [104] . The remodelling in asthmatic lungs is in part caused by collagen and proteoglycan secretion from interstitial fibroblasts. Eosinophils have been suggested to participate in this by secretion of transforming growth factor (TGF) beta [105, 106] but here is additionally described how ECP could influences fibrosis development. Stimulation of a human fetal lung fibroblast cell line (HFL1) with moderate/high levels of ECP (5-10 μg/mL) for 24-48 hr resulted in increased release of TGF-beta [81] . ECP also augmented fibroblast mediated contraction of collagen gel and stimulated migration of HFL1 fibroblasts which could be blocked with antibodies to ECP [107] . In addition, ECP incubated with the fibroblast cell line for 6 hr resulted in a 6-fold increase of intracellular proteoglycan accumulation [108] .