American Journal of Reproductive Immunology · 1990 · 64 citations · 23 references
Life SciencesImmunologyPharmacologyImmunoregulationInflammationInnate ImmunityAnti-inflammatory PharmacologyCytokine BiologyInflammatory Cell ResponsesInflammatory MediatorsInflammatory SignalingSteroid PharmacologyAnti-inflammatory MechanismsInflammatory ActivationInflammatory Cytokine EffectsPro-inflammatory Mediator SignalingProgesterone ImmunomodulationProgesterone-mediated Immune Modulation
The effects of estradiol (E2), progesterone (P), and danazol on the production of interleukin-1 beta (IL-1 beta) and tumor necrosis factor (TNF) by OK-432 (a streptococcal preparation)-stimulated monocytes were examined. E2 and P at physiologic concentrations enhanced IL-1 beta and TNF production by monocytes from donors with lower control levels (without steroids added) of IL-1 beta and TNF. However, E2 and P at physiologic concentrations did not affect IL-1 beta and TNF production by monocytes from donors with higher control levels of IL-1 beta and TNF. Danazol inhibited IL-1 beta and TNF production by monocytes in a dose-dependent manner from not only donors with lower control levels of IL-1 beta and TNF but also donors with higher control levels of IL-1 beta and TNF. Danazol at a concentration of 10(-6) M significantly suppressed IL-1 beta and TNF production in the presence of E2 and/or P at concentrations giving peak responses of IL-1 beta production. These findings suggest possible new mechanisms of action for danazol in the treatment of endometriosis and infertility associated with immune abnormalities.
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