Fibrosis is part of airway remodelling observed in bronchial asthma and COPD. Pro-fibrotic activity of lung fibroblasts may be suppressed by β-adrenoceptor activation. We aimed, first, to characterise the expression pattern of β-adrenoceptor subtypes in human lung fibroblasts and, second, to probe β-adrenoceptor signalling with an emphasis on anti-fibrotic actions. Using reverse transcription PCR, messenger RNA (mRNA) encoding β 2 -adrenoceptors was detected in MRC-5, HEL-299 and primary human lung fibroblasts, whereas transcripts for β 1 -and β 3 -adrenoceptors were not found. Real-time measurement of dynamic mass redistribution in MRC-5 cells revealed β-agonistinduced G s -signalling. Proliferation of MRC-5 cells (determined by [ 3 H]-thymidine incorporation) was significantly inhibited by β-agonists including the β 2 -selective agonist formoterol (−logIC 50 , 10.2) and olodaterol (−logIC 50 , 10.6). Formoterol's effect was insensitive to β 1 -antagonism (GCP 20712, 3 μM), but sensitive to β 2 -antagonism (ICI 118,551; apparent, pA 2 , 9.6). Collagen synthesis in MRC-5 cells (determined by [ 3 H]-proline incorporation) was inhibited by β-agonists including formoterol (−logIC 50 , 10.0) and olodaterol (−logIC 50 , 10.3) in a β 2 -blockersensitive manner. α-Smooth muscle actin, a marker of myofibroblast differentiation, was down-regulated at the mRNA and the protein level by about 50% following 24 and 48 h exposure to 1 nM formoterol, a maximally active concentration. In conclusion, human lung fibroblasts exclusively express β 2 -adrenoceptors and these mediate inhibition of various markers of pro-fibrotic cellular activity. Under clinical conditions, anti-fibrotic actions may accompany the therapeutic effect of long-term β 2 -agonist treatment of bronchial asthma and COPD.