Overproduction of multiple proinflammatory mediators (CCL-2, TNF-α, IL-1β, IL-6), triggered by different stimuli (IL-1β, LPS and IFN-γ) in fibroblasts from different (lung and dermal) origins, denotes that the proinflammatory status in CF fibroblasts is a ubiquitous, extensive and complex process involving multiple signalling pathways and transcription factors that may act separately or in concert. This evidence concerns the gene IL1B and cystic fibrosis.