Gonadal steroids modulate human monocyte interleukin-1 (IL-1) activity.

Interleukin-1 (IL-1), a monocyte and macrophage product, is the mediator of a wide variety of immune responses, including fever, and increases during the luteal phase of the menstrual cycle, concomitantly with progesterone (P). These studies were undertaken to assess the possible relationship between steroidogenesis and IL-1 activity elaborated by human peripheral monocytes. IL-1 was measured with the D-10 thymocyte stimulation bioassay and dose response curves as a function of both estradiol (E2) and P were established. Low concentrations of both E2 (10(-9) M-10(-10) M) and P (10(-8) M-10(-9) M) resulted in maximal IL-1 stimulation. At higher concentrations of both E2 (10(-7) M) and P (10(-7) M-10(-5) M) there was a significant reduction (P less than 0.05) in IL-1 activity. However, neither E2 nor P production by human granulosa-luteal cells cultured with increasing amounts of human IL-1 (0 to 20 IU/ml) was affected in either the absence or presence of human chorionic gonadotropin (hCG, 5 IU/ml). Thus, human peripheral monocyte IL-1 activity appears to be modulated by gonadal steroids; however, a reciprocal relationship between IL-1 and gonadal steroidogenesis was not observed.