Journal
INFLAMMATORY BOWEL DISEASES
Volume 10, Issue 2, Pages 122-128Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00054725-200403000-00010
Keywords
anti-inflammatory effects; butyrate; human endothelial cells; inflammatory bowel disease (IBD); nuclear factor kappaB (NF-kappa B); short-chain fatty acids; vascular cell adhesion molecule (VCAM)
Categories
Ask authors/readers for more resources
Background: Leukocyte recruitment to areas of inflammation depends on Integrin-VCAM/ICAM interaction. Blocking the vascular cell adhesion molecule (VCAM-1) and the intracellular adhesion molecule (ICAM-1) may have therapeutic benefit for the inflammatory component of bowel disease. Notably, the induction of ICAM and VCAM is mediated by a nuclear factor kappaB (NF-kappaB)- dependent mechanism. We investigated whether the antiinflammatory properties of butyrate are mediated via the modulation of VCAM and ICAM on human endothelial cells. Methods: VCAM-1 and ICAM-1 expression on human endothelial cells upon tumor necrosis factor-alpha (TNF-alpha) stimulation was assessd by FACS analysis. A monocyte adhesion assay was performed to evaluate the relevance of a modulated CAM-expression. Electrophoretic mobility shift assays were applied to investigate NF-kappaB activation. Results: The observed butyrate-associated inhibition of monocyte adhesion to endothelial cells is associated with an inhibition of NF-kappaB activation in human endothelial cells. In this context, the observed suppression of the TNF-alpha induced VCAM-1 expression is likely to play an essential role. Conclusions: Butyrate inhibits VCAM-1 mediated leukocyte adhesion to human endothelial cells. This inhibition may contribute to the anti-inflammatory effects of butyrate in patients with distal ulcerative colitis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available