This study reports peripheral changes in GM-CSF-producing CD4<sup>+</sup> T cells in septic patients and the possible underlying mechanism by which GM-CSF influences the outcome of sepsis.
In the present study we evaluated the ability of granulocyte macrophage-colony stimulating factor (GM-CSF) to mobilize BMDPC in a lipopolysaccharide (LPS)-induced sepsis model and thereby its potential as a novel treatment strategy.
Trials assessing the therapeutic benefit of IL-7, granulocyte-macrophage colony-stimulating factor (GM-CSF) and antibodies against programmed cell death protein 1 (PD1) and programmed cell death 1 ligand 1 (PDL1) for the treatment of sepsis are in progress.
CSF glucose levels in infants with possible sepsis were 2.71 (SD 0.83) mmol/l and not significantly different from infants without sepsis with 2.55 mmol/l (SD 0.34).
Despite treatment with granulocyte-macrophage--colony-stimulating factor, the marrow transplant recipient remained neutropenic and died of polymicrobial sepsis and aspergillosis 38 days after the transplant.