| Abstrakt: |
IL-11, a new hematopoietic cytokine isolated from primate stromal cells (PU-34), has been shown to act synergistically with IL-3 to induce proliferation of early hematopoietic stem cells and induce in vitroCFU-MEG proliferation. We hypothesize that recombinant human (rh)IL-11 alone or in combination with granulocyte colony-stimulating factor (G-CSF) might modulate newborn in vivogranulopoiesis and thrombopoiesis. Newborn Sprague-Dawley rats were given 14 d of intraperitoneal rhIL-11 (0–250 μg/kg × 14 d), rhIL-11 (250 μg/kg) rhG-CSF (5 μg/kg simultaneously × 14 d), rhIL-11 ± 7 d followed by G-CSF × 7 d, G-CSF × 14 d, PBS/human serum albumin × 7 d followed by G-CSF × 7 d, or PBS/human serum albumin × 14 d. rhIL-11 alone had no effect on the circulating hematocrit or absolute neutrophil count. There was, however, a significant increase in the circulating platelet count after rhIL-11 (100 and 250 μg/kg) versus PBS/ human serum albumin (d 13:1241 ± 54, 1262 ± 58 versus 939 ± 38 k/mm3; p= 0.01). Sequential and simultaneous IL-11 G-CSF caused a significant increase in the marrow neutrophil reserve and the circulating absolute neutrophil count above that observed when G-CSF alone was administered. IL-11 ± G-CSF, however, failed to reduce the 96-h mortality rate during experimental group B streptococcal sepsis. These data suggest that IL-11 alone results in a significant elevation in the blood platelet concentration and, in combination with G-CSF, induces an increase in in vivo neonatal rat myelopoiesis. This novel cytokine may have the potential to decrease the morbidity associated with cytopenias in the newborn. |
