z-logo
open-access-imgOpen Access
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).

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom