n-Butyrate inhibits Jun NH(2)-terminal kinase activation and cytokine transcription in mast cells
- Institute of Immunology, Medical University of Vienna, Borschkegasse 8a, A-1090 Vienna (Austria)
- Department of Autoimmune and Inflammatory Bowel Diseases, Novartis Institute for BioMedical Research, Brunnerstrasse 53, A-1235 Vienna (Austria)
- Department of Internal Medicine III, Division of Nephrology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna (Austria)
Mast cells are well known to contribute to type I allergic conditions but only recently have been brought in association with chronic relapsing/remitting autoimmune diseases such as celiac disease and ulcerative colitis. Since the bacterial metabolite n-butyrate is considered to counteract intestinal inflammation we investigated the effects of this short chain fatty acid on mast cell activation. Using RNAse protection assays and reporter gene technology we show that n-butyrate downregulates TNF-{alpha} transcription. This correlates with an impaired activation of the Jun NH(2)-terminal kinase (JNK) but not other MAP kinases such as ERK and p38 that are largely unaffected by n-butyrate. As a consequence, we observed a decreased nuclear activity of AP-1 and NF-AT transcription factors. These results indicate that n-butyrate inhibits critical inflammatory mediators in mast cells by relatively selectively targeting the JNK signalling.
- OSTI ID:
- 20854535
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 349, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2006.08.117; PII: S0006-291X(06)01939-5; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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