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J. Biol. Chem., Vol. 276, Issue 48, 44641-44646, November 30, 2001
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From the Department of Molecular and Cellular Biology, University
of Connecticut, Storrs, Connecticut 06269
Butyrate is derived from the microbial metabolism
of dietary fiber in the colon where it plays an important role in
linking colonocyte turnover and differentiation to luminal content. In addition, butyrate appears to have both anti-inflammatory and cancer
chemopreventive activities. Using confocal microscopy and cell
fractionation studies, butyrate pretreatment of a human colon cell line
(HT-29 cells) inhibited the tumor necrosis factor-
Butyrate Suppression of Colonocyte NF-
B Activation and
Cellular Proteasome Activity*
(TNF-)-induced
nuclear translocation of the proinflammatory transcription factor
NF-
B. Butyrate inhibited NF-B DNA binding within 30 min of
TNF- stimulation, consistent with an inhibition of nuclear translocation. IB·NF-B complexes extracted from
butyrate-treated cells were relatively resistant to in
vitro dissociation by deoxycholate, suggesting a change in
cellular IB composition. Butyrate treatment increased p100
expression, an IB that was not degraded upon TNF- treatment.
Butyrate also reduced the extent of TNF--induced IB- degradation and enhanced the presence of ubiquitin-conjugated IB-. The suppression of IB- degradation corresponded with a
reduction in cellular proteasome activity as determined by in vitro proteasome assays and the increased presence of
ubiquitin-conjugated proteins. The butyrate suppression of IB-
degradation and proteasome activity may derive from its ability to
inhibit histone deacetylases since the specific deacetylase inhibitor
trichostatin A had similar effects. These results suggest a potential
mechanism for the anti-inflammatory activity of butyrate and
demonstrate the interplay between short chain fatty acids and cellular
proteasome activity.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Molecular and
Cell Biology, 75 North Eagleville Rd., U-125, University of
Connecticut, Storrs, CT 06269. Tel.: 860-486-0454; Fax: 860-486-4331; E-mail: Giardina@uconnvm.uconn.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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