FK506 and cyclosporin A inhibit granulocyte/macrophage colony-stimulating factor production by mononuclear cells in asthma.

Bronchial asthma is associated with eosinophilic inflammation and expression of T-cell-derived cytokines, which influence eosinophilic function. FK506, a newly established immunosuppressive agent, may have potential as a therapeutic instrument for asthma because of its suppressive effect on T-cell activation. To assess this, we compared the inhibitory effects of FK506 and cyclosporin A on production of granulocyte/macrophage colony-stimulating factor and interleukin-5 by interleukin-2- or Dermatophagoides farinae-stimulated mononuclear cells from patients with asthma, and their contribution to proliferation and survival of eosinophils in vitro. FK506 inhibited granulocyte/macrophage colony-stimulating factor production by stimulated mononuclear cells from asthma patients at lower concentrations than cyclosporin A. Both drugs inhibited eosinophil proliferation and survival activity from mononuclear cells at comparable concentrations. Interleukin-5 production by stimulated mononuclear cells was also inhibited both by FK506 and cyclosporin A. We conclude that both FK506 and cyclosporin A have potential for therapy of bronchial asthma.