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Possible role of tumor necrosis factor‐alpha in erythropoietic suppression by endotoxin and granulocyte/macrophage colony‐stimulating factor
Author(s) -
Udupa K. B.,
Sharma B. G.
Publication year - 1996
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199607)52:3<178::aid-ajh7>3.0.co;2-q
Subject(s) - tumor necrosis factor alpha , granulocyte , granulocyte macrophage colony stimulating factor , granulocyte macrophage colony stimulating factor receptor , medicine , immunology , tumor necrosis factor α , granulocyte colony stimulating factor , macrophage , cancer research , biology , cytokine , macrophage colony stimulating factor , chemotherapy , in vitro , biochemistry
Injection of bacterial endotoxin or granulocyte/macrophage colony‐stimulating factor (GM‐CSF) into exhypoxic polycythemic mice simultaneously with erythropoietin (EPO) suppressed erythroid cell formation, as monitored by 59 Fe incorporation into circulating red blood cells. This effect was dose‐dependent and time‐dependent. GM‐CSF did not inhibit erythroid cell formation directly, as the antibody to the GM‐CSF did not neutralize the effect of endotoxin, the inducer of GM‐CSF. The suppression of both agents could be partially corrected by prior injection of a monoclonal antibody to tumor necrosis factor α (anti‐TNFα). These results indicate that the suppression of EPO‐induced erythroid cell formation by endotoxin and GM‐CSF was due in part to the production of TNFα. © 1996 Wiley‐Liss, Inc.