Inhibitor κB and Nuclear Factor κB in Granulocyte‐Macrophage Colony‐Stimulating Factor Antagonism of Dexamethasone Suppression of the Macrophage Response toAspergillus fumigatusConidia
Author(s) -
JungHyun Choi,
Elmer Brummer,
Young Jun Kang,
Patricia P. Jones,
David A. Stevens
Publication year - 2006
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/500948
Subject(s) - aspergillus fumigatus , antagonism , microbiology and biotechnology , macrophage , dexamethasone , aspergillus , biology , granulocyte macrophage colony stimulating factor receptor , immunology , macrophage colony stimulating factor , in vitro , biochemistry , endocrinology , receptor
The dexamethasone (DEX) immunosuppressive effect on macrophage killing activity and cytokine production in response to Aspergillus fumigatus conidia is antagonized by granulocyte-macrophage colony-stimulating factor (GM-CSF). The molecular mechanism is unknown. We postulated that this antagonism is mediated by inhibitor kappaB (I kappaB) induction by DEX and is opposed by acceleration of I kappaB degradation by GM-CSF with or without conidia stimulation, with corresponding effects on translocation and activation of nuclear factor kappa B (NF-kappaB).
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