Butyrate modulates gene and protein expression in human intestinal endothelial cells. Biochem Biophys Res Commun 2003 Sep 26;309(3):512-9
Date
09/10/2003Pubmed ID
12963019DOI
10.1016/j.bbrc.2003.08.026Scopus ID
2-s2.0-0041829406 (requires institutional sign-in at Scopus site) 58 CitationsAbstract
We hypothesized that sodium butyrate, a product of enteric bacterial fermentation, modulates gene expression in gut microvascular endothelium which plays a central role in mucosal immunity. We examined sodium butyrate's effect on LPS-induced gene and protein expression in primary cultures of human intestinal microvascular endothelial cells. cDNA array analysis revealed that sodium butyrate augmented ICAM-1 mRNA expression, while it inhibited IL-6 and COX-2 expression in response to LPS stimulation. These results were confirmed at the protein level. Prostaglandin E2 production by LPS was also strongly inhibited by butyrate. The pattern of altered gene expression by butyrate was reproduced by the histone deacetylase inhibitor tricostatin A, suggesting that the regulatory mechanism of butyrate on HIMEC gene expression involves histone deacetylase inhibition. IkappaBalpha degradation and NF-kappaB activation were unaffected by butyrate. In addition to effects on epithelium, sodium butyrate modulates the innate mucosal immune response towards LPS through effects on microvascular endothelial function.
Author List
Ogawa H, Rafiee P, Fisher PJ, Johnson NA, Otterson MF, Binion DGAuthor
Mary F. Otterson MD Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
ButyratesCells, Cultured
Cyclooxygenase 2
Dinoprostone
E-Selectin
Endothelium, Vascular
Gene Expression Regulation
Humans
I-kappa B Proteins
Intercellular Adhesion Molecule-1
Interleukin-6
Intestines
Isoenzymes
Lipopolysaccharides
Membrane Proteins
Microcirculation
NF-KappaB Inhibitor alpha
NF-kappa B
Prostaglandin-Endoperoxide Synthases
