Colonic epithelial cells induce endothelial cell expression of ICAM‐1 and VCAM‐1 by a NF‐κB‐dependent mechanism

• Published in: Clinical and experimental immunology 2001-05, Vol.124 (2), p.208-213
• Main Authors: Maaser, C., Schoeppner, S., Kucharzik, T., Kraft, M., Schoenherr, E., Domschke, W., Luegering, N.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Caco‐2; Fundamental and applied biological sciences. Psychology; g-Interferon; Gut Immunology; HMEC‐1; HUVEC; IFN‐γ; Inflammation; intercellular adhesion molecule 1; Molecular and cellular biology; NF-B protein; TNF‐α; vascular cell adhesion molecule 1
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1046/j.1365-2249.2001.01541.x

Epithelial cells are positioned in close proximity to endothelial cells. A non‐contact coculture system was used to investigate whether colonic epithelial cells activated with various cytokines are able to provide signals that can modulate ICAM‐1 and VCAM‐1 expression on endothelial cells. Coculture of human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC‐1) with TNF‐α/IFN‐γ‐stimulated human colon epithelial cell lines led to a significant up‐regulation of endothelial ICAM‐1 and VCAM‐1 expression. Increased ICAM‐1 and VCAM‐1 expression by endothelial cells was accompanied by an increase in endothelial cell NF‐κB p65 and NF‐κB‐DNA‐binding activity. Inhibition of endothelial NF‐κB activation using the proteosome inhibitors MG‐132 and BAY 11–7082 resulted in a significant decrease of ICAM‐1 expression, indicating an important role for NF‐κB in this response. This cross‐talk may represent a biological mechanism for the gut epithelium to control the colonic inflammatory response and the subsequent immune cell recruitment during inflammation.