Regulatory roles of burst-promoting activity (BPA) from bone marrow cells during human regenerating hemopoiesis.

To clarify the regulatory roles of burst-promoting activity (BPA) in cases of in vivo erythropoiesis, we examined erythroid progenitors and BPA in 18 patients with a regenerating hemopoiesis following intensive chemotherapy. Marrow erythroid progenitors increased remarkably in these patients. Bone marrow-conditioned medium (BMCM) and sera obtained from these patients revealed high levels of BPA. Serial examination of a typical case showed that BPA in BMCM and sera increased during regenerating hemopoiesis, but decreased when the hemopoiesis stabilized. Adherent cell depletion and treatment with monoclonal antibody (OKM1) reduced BPA production from the bone marrow cells, thereby suggesting that bone marrow macrophages are responsible for the BPA production. Fractionation of pooled BMCM with Amicon Diaflo membranes showed that the BPA was mainly present in the 30,000- to 50,000-dalton fraction. BPA in BMCM was heat labile, inactivated by trypsin and protease, but was not inactivated by neuraminidase. Pooled BMCM did not influence the growth of CFU-E-derived colonies. Our results suggest that to repair disturbed erythropoiesis, bone marrow macrophages produce BPA during regenerating hemopoiesis.