Increased interleukin‐8 release by β‐adrenoceptor activation in human transformed bronchial epithelial cells

1 The effect of β‐adrenoceptor activation on release of the neutrophil chemoattractant, interleukin‐8 (IL‐8), was examined in human transformed bronchial epithelial cells (16HBE cells). 2 The combined β 1 ‐ and β 2 ‐adrenoceptor agonist, isoprenaline, time‐ (100 nM, 2–18 h) and concentration‐ (1–30 nM) dependently increased IL‐8 protein content in the cell culture supernatant as measured by an enzyme immunosorbent assay standardized for DNA by fluoro‐colorimetry. 3 Isoprenaline (1–100 nM, 15 min) increased cyclic AMP concentration‐dependently. 4 The effect of isoprenaline (100 nM) was inhibited by the β‐adrenoceptor blocker propranolol (10 μ m ). The maximum magnitude of IL‐8 increase caused by β‐adrenoceptor activation was 40% of that caused by the pro‐inflammatory cytokine tumor necrosis factor‐alpha (TNF‐α: 100 ng ml −1 ). 5 The selective β 2 ‐adrenoceptor agonist salbutamol (1 μ m ), increased IL‐8 protein similarily to isoprenaline and the cyclic AMP analogue, dibutyryl cyclic AMP (1 mM) produced a corresponding effect. 6 Pretreatment with isoprenaline (100 nM) followed by TNF‐α (20 ng ml −1 ) increased IL‐8 additively. 7 In conclusion, β‐adrenoceptor stimulation increased the release of the neutrophil chemoattractant, IL‐8 in 16HBE cells, via an increase in intracellular cyclic AMP. β‐adrenoceptor stimulation adds to the IL‐8 increase caused by the pro‐inflammatory cytokine TNF‐α. If this mechanism exists in vivo , β‐adrenoceptor activation may increase neutrophil chemotaxis into the airways.