In vivoex vivo Studies

G-CSF is produced by macrophages, fibroblasts, and endothelial cells in virtually all organs in the body. It exerts its biological actions on precursors as well as on mature PMNs. In particular, G-CSF increases the number of circulating neutrophils, by stimulating the proliferation and differentiation of myeloid progenitor cells, and moreover enhances their phagocytic activity (Antachopoulos and Roilides, 2005). Administration of G-CSF in neutropenic animal models of invasive candidiasis, aspergillosis, or trichosporonosis was associated with faster recovery from neutro-penia and improved survival (Hamood et al., 1994; Muranaka et al., 1997; Graybill et al., 1998). Consequently, theoretically, the administration of G-CSF would be beneficial in resolving scedosporiosis. No animal model studies have reported on the effects of G-CSF on the outcome of experiment fusariosis up to date. Ortoneda et al., in an immunosuppressed murine model of invasive infection by S. prolificans, demonstrated a modest efficacy of liposomal amphotericin B (LAMB) at 10 mg/kg/ day combined with G-CSF (Ortoneda et al., 2002a). Subsequent studies showed that LAMB at very high doses (40 mg/kg/day) combined with G-CSF did not significantly improve the survival (Ortoneda et al., 2004). Interestingly, administration of G-CSF alone, was not more effective as compared to the control group (Ortoneda et al., 2004; Ortoneda et al., 2002a). In an immunocompetent murine model of disseminated S.prolificans infection it has been shown that posaconazole and GM-CSF have a combined effect in damaging S. prolificans hyphae ex vivo. However, when posaconazole and GM-CSF were administered to mice with invasive infection due to S. prolificans, they had selective beneficial effects on the burdens in certain organs but offered no additional benefit to survival (Simitsopoulou et al., 2004).

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