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Inflamm Bowel Dis ; 10(2): 122-8, 2004 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15168812

RESUMO

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 anti-inflammatory 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.


Assuntos
Butiratos/farmacologia , Endotélio Vascular/citologia , Molécula 1 de Adesão Intercelular/biossíntese , Fator de Necrose Tumoral alfa/farmacologia , Molécula 1 de Adesão de Célula Vascular/biossíntese , Células Cultivadas , Interações Medicamentosas , Ensaio de Desvio de Mobilidade Eletroforética , Endotélio Vascular/efeitos dos fármacos , Citometria de Fluxo , Humanos , Molécula 1 de Adesão Intercelular/efeitos dos fármacos , Sensibilidade e Especificidade , Molécula 1 de Adesão de Célula Vascular/efeitos dos fármacos
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