Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IL-33-induced cytokine production in primary mouse mast cells
| Autor: | Anuya Paranjape, Marcela T. Taruselli, Amina Abdul Qayum, Andrew J. Spence, John J. Ryan, Heather L. Caslin, Jamie Josephine Avila McLeod, Elizabeth Motunrayo Kolawole, Howard L. Elford |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Male medicine.medical_treatment Immunology Primary Cell Culture Bone Marrow Cells Immunoglobulin E Hydroxamic Acids Article Allergic inflammation 03 medical and health sciences Mice Genes Reporter medicine Animals Hydroxyurea Mast Cells Luciferases Chemokine CCL3 Interleukin-13 biology Tumor Necrosis Factor-alpha NF-kappa B NFKB1 Interleukin-33 Acetylcysteine Interleukin 33 Mice Inbred C57BL Transcription Factor AP-1 030104 developmental biology Cytokine Ribonucleotide reductase Gene Expression Regulation Interleukin 13 biology.protein Cancer research Tumor necrosis factor alpha Female Immunosuppressive Agents Signal Transduction |
| Zdroj: | Cellular immunology. 319 |
| ISSN: | 1090-2163 |
| Popis: | While IgE is considered the primary mediator of mast cell activation, IL-33 contributes substantially in asthma, allergic rhinitis, and atopic dermatitis. To develop effective treatments for allergic disease, it is important to understand the role of therapeutic agents on IL-33 activation. We examined the effect of Didox (3,4-dihydroxybenzohydroxamic acid), an antioxidant and ribonucleotide reductase (RNR) inhibitor, on IL-33-mediated mast cell activation. Didox suppressed IL-6, IL-13, TNF, and MIP-1α (CCL3) production in bone marrow derived mast cells following IL-33 activation. This suppression was observed in different genetic backgrounds and extended to peritoneal mast cells. The antioxidant N-acetylcysteine mimicked the suppression of Didox, albeit at a much higher dose, while the RNR inhibitor hydroxyurea had no effect. Didox substantially suppressed IL-33-mediated NFκB and AP-1 transcriptional activities. These results suggest that Didox attenuates IL-33-induced mast cell activation and should be further studied as a potential therapeutic agent for inflammatory diseases involving IL-33. |
| Databáze: | OpenAIRE |
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