The effects of β2‐adrenoceptor agonists and a corticosteroid, budesonide, on the secretion of inflammatory mediators from monocytes

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Abstract
1 The in vitro effects of the β2-adrenoceptor agonists (1 × 10−9−10−5 m), terbutaline, salmeterol, and formoterol, on the release of inflammatory mediators, i.e. the eicosanoids leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) and the cytokine interleukin-1β (IL-1β), were assessed in cultures of human blood monocytes. For comparison, the effects of a 5-lipoxygenase inhibitor, BW A4C (1 × 10−9−10−5 m), and a corticosteroid, budesonide (1 × 10−10−10−5 m) were also examined. Sotalol was used to investigate whether the actions of β2-agonists were mediated through β-adrenoceptors. 2 Terbutaline, like budesonide, had no significant effect on LTB4 release, whereas BW A4C (IC50 = 2 × 10−8 m) was a potent inhibitor. All concentrations of formoterol approximately halved the LTB4 secretion, whereas high concentrations (1 × 10−7−10−5 m) only, of salmeterol, inhibited release. Only salmeterol, at high concentrations (> 1 × 10−6 m), lowered the secretion of PGE2 in monocyte cultures. Formoterol and salmeterol reduced the secretion of IL-1β only at the highest dose (1 × 10−5 m). In contrast, budesonide (≥ 1 × 10−9 m) was a potent suppressant of this secretion. 3 Treatment of monocyte cultures with sotalol (1 × 10−5 m) did not significantly antagonize the inhibitory effects of salmeterol and formoterol. These results suggest that the inhibitory action of these β2-agonists on the release of eicosanoids or IL-1β, is not mediated via β2-adrenoceptors. 4 This study does not support a therapeutic importance of the anti-release effects of β2-agonists since high concentrations were generally required. Furthermore, the anti-secretory action of β2-agonists was distinct from that of corticosteroids.

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