Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IL-33-induced cytokine production in primary mouse mast cells

•Didox suppresses IL-33-induced mast cell cytokine production.•Didox-mediated suppression is 100-fold more potent than N-acetylcysteine effects.•Didox attenuates NFκB and AP-1 transcriptional activities. While IgE is considered the primary mediator of mast cell activation, IL-33 contributes substant...

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Veröffentlicht in:	Cellular immunology 2017-09, Vol.319, p.10-16
Hauptverfasser:	Caslin, Heather L., McLeod, Jamie Josephine Avila, Spence, Andrew J., Qayum, Amina Abdul, Kolawole, Elizabeth Motunrayo, Taruselli, Marcela T., Paranjape, Anuya, Elford, Howard L., Ryan, John J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetylcysteine - pharmacology Allergic inflammation Animals AP-1 Bone Marrow Cells - cytology Bone Marrow Cells - drug effects Bone Marrow Cells - immunology Chemokine CCL3 - antagonists & inhibitors Chemokine CCL3 - genetics Chemokine CCL3 - immunology Didox Female Gene Expression Regulation - drug effects Gene Expression Regulation - immunology Genes, Reporter Hydroxamic Acids - pharmacology Hydroxyurea - pharmacology IL-33 Immunosuppressive Agents - pharmacology Interleukin-13 - antagonists & inhibitors Interleukin-13 - genetics Interleukin-13 - immunology Interleukin-33 - antagonists & inhibitors Interleukin-33 - pharmacology Lipopolysaccharides - pharmacology Luciferases - genetics Luciferases - immunology Male Mast cells Mast Cells - cytology Mast Cells - drug effects Mast Cells - immunology Mice Mice, Inbred C57BL NF-kappa B - antagonists & inhibitors NF-kappa B - genetics NF-kappa B - immunology NFκB Primary Cell Culture Signal Transduction Transcription Factor AP-1 - antagonists & inhibitors Transcription Factor AP-1 - genetics Transcription Factor AP-1 - immunology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology
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