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Protective effect of granulocyte‐colony stimulating factor against amphotericin B‐induced myelosuppression in vitro
Author(s) -
Charak Bishan S.,
Brown Ernest G.,
Mazumder Amitabha
Publication year - 1994
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1994.tb05106.x
Subject(s) - amphotericin b , granulocyte colony stimulating factor , granulocyte , monoclonal antibody , bone marrow , in vitro , immunology , cytokine , in vivo , myeloid , tumor necrosis factor alpha , medicine , pharmacology , chemotherapy , antibody , biology , biochemistry , antifungal , microbiology and biotechnology , dermatology
Summary Amphotericin B causes suppression of bone marrow (BM) progenitor cells in vitro . Granulocyte colony stimulating factor (G‐CSF) enhances the proliferation of myeloid cells. The present study defines the role of G‐CSF in preventing amphotericin B‐induced myelosuppression. G‐CSF increased the proliferative potential of BM and protected against amphotericin B‐induced myelosuppression if it was added to the medium during the early phase of exposure of BM to amphotericin B. Monoclonal antibodies to tumour necrosis factor‐α (TNF) or interferon‐γ (IFN) inhibited the myelosuppression partially: simultaneous presence of both these antibodies completely abrogated this suppression, suggesting that both TNFα and IFNγ were involved in amphotericin‐induced myelosuppression. TNF‐ or IFN‐ induced suppression of BM was also inhibited by G‐CSF. These data suggest that G‐CSF prevents the amphotericin B‐induced myelosuppression by antagonizing the suppressive effects of TNF and IFN and by enhancing the proliferative activity of BM.