Effects of rhIL-1 alpha, rhIL-1 beta, and rhIL-1 receptor antagonist on erythroid progenitors (CFU-E and BFU-E) in human bone marrow.

Interleukin-1 (IL-1) is known to promote the production of colony-stimulating factor (CSF) and to possess the ability to protect the bone marrow suppression in granulocyte-macrophage (GM) series associated with radiotherapy or chemotherapy. There are conflicting reports concerning the action of IL-1 on erythroid progenitors, however, and no consensus has been established. In the present study, the influences of recombinant human IL-1 alpha (rhIL-1 alpha), rhIL-1 beta, and rhIL-1 receptor antagonist (rhIL-1ra) on erythroid progenitors (colony-forming units-erythroid, CFU-E; and burst-forming units-erythroid, BFU-E) in human bone marrow were studied. rhIL-1 alpha and rhIL-1 beta (1-1000 pg/mL) enhanced the CFU-E and BFU-E growth in human nonadherent (NA) bone marrow cells. rhIL-1 alpha and rhIL-1 beta also stimulated the formation of CFU-E and BFU-E in the NA and T cell-depleted bone marrow fraction. Moreover, rhIL-1 alpha and rhIL-1 beta enhanced the CFU-E and BFU-E in the CD34+ bone marrow cell fraction. These data and the results of limiting dilution analysis indicate that the stimulatory effect of IL-1 may consist of direct actions on erythroid progenitors. The enhancing effect of rhIL-1 alpha and rhIL-1 beta on erythroid progenitors was inhibited by rhIL-1ra. These data suggest that the stimulatory effect of IL-1 on CFU-E and BFU-E is mediated via the IL-1 receptor.