ABSTRACT
It has been postulated that interleukin-lα (IL-lα) and interleukin-1ß (IL-1ß) play a role in the pathogenesis of the anemia of chronic disease by inhibiting the proliferation of human erythroid progenitor cells. In the course of investigating this hypothesis we found that IL-1 type I receptor (IL-1R) mRNA is expressed on erythroid progenitor enriched, primitive human hematopoietic cells (CD34+, c-kit-R(bright)) and on cells isolated from human erythroid burst forming colonies (BFU-E). Nevertheless, when CD34+, c-kit-R(bright) cells were exposed to IL-1α and IL-1ß in vitro, cloning efficacy of BFU-E and CFU-E in a serum free culture system was not inhibited. Moreover, in apparent contradiction to the hypothesis being tested, we found that both IL-1 isoforms actually increased the survival of human BFU-E in serum free, growth factor free medium. Accordingly, these results suggest that if IL-1 plays a role in the pathogenesis of the anemia of chronic disease, it is not due to a direct suppressive effect on erythroid cell growth. Rather, our data support the hypothesis that IL-1 may cause the elaboration of another inhibitory cytokine (s) by cells of the marrow microenvironment.