Parenchymal fibroblasts in COPD display reduced proliferation [75], reduced capability to sustain tissue repair (increased PGE2 production and EP2/EP4 expression, reduced response to TGFβ) [76], reduced contractility [76,77], reduced migration to chemoattractants [76] and increased expression and secretion of CXCL8 and IL-6 [78]. This evidence concerns the gene CXCL8 and chronic obstructive pulmonary disease.