Impact of experimental peritonitis on bone marrow cell function

Background. The effects of abdominal sepsis on the regulation of cell turno ver in bone marrow and on the function of hematopoietic stem cells were inv estigated. Methods. In a new mouse model of abdominal sepsis (colon ascendens stent pe ritonitis [CASP]) the proliferation, apoptosis, and colony-forming capacity of bone marrow cells were determined. Results. Both experimental peritonitis and sham surgery increased prolifera tion of bone marrow cells significantly (P <.01). Incubation with granulocy te-macrophage colony-stimulating factor bat not granulocyte colony-stimulat ing-factor further augmented proliferation of bone marrow cells from septic mice. In contrast to cell proliferation, bone marrow cell apoptosis was si gnificantly (P <. 001) increased in response to CASP but not to sham surger y. CASP surgery and treatment of normal bone marrow cells with lipopolysacc haride, tumor necrosis factor-alpha, interleukin 1 beta, and interferon gam ma increased the number of apoptotic cells to a similar extent. Stem cell a ssays revealed that during the late phase of peritonitis the colony formati on by granulocytic-monocytic precursors was increased, whereas mature eryth roid colony-forming cells were suppressed. Incubation of normal bone marrow cells with lipopolysaccharide and cytokines showed similar effects. Conclusions. These results reveal differential effects of experimental peri tonitis on various hematopoietic lineages and suggest a potential role of i nflammatory mediators for the dysregulation of bone marrow cell function du ring abdominal sepsis.