An imbalance of functional interactions between nutrient-sensing nuclear receptors (e.g. Vitamin D receptor, VDR) and stress-sensing transcription factors (e.g. NF-kappaB, NFkB) induced by lifetime exposure to micronutrients and cytokines may be a central molecular process towards atherosclerosis. We wanted to highlight potential interactions between VDR and NFkB signalling in vascular endothelial cells, the first cell population implicated in this disease. Microarray analyses were carried out on total RNA extracted from EA.hy926 (human umbilical vein endothelial cells line) after stimulation with TNFalpha (TNF) and/or 1-alpha 25(OH)2 vitamin D3 (VD) up to 24h. Transformation/normalisation of raw data (Bioconductor software) delineated a variety of genes regulated by TNF or by VD alone, or by TNF and VD in a synergistic or antagonistic way. We focused on the genes regulated by TNF and VD in an opposite way and identified a group of genes potentially implicated in macrophage chemo-attraction (Chemokine (C-C motif) ligand 2, 4 and 5 (CCL2, 4 and 5)): they were up-regulated by TNF and these up-regulations are reduced by VD. Microarray data were further verified and confirmed by real time RT-PCR for CCL2, 4 and 5. Also, the effect of VD was abolished when VDR expression was switched off by siRNA. The same results were obtained when cycloheximide was added to the TNF and VD treatment. The implication of VDR seems however to be indirect and to involve a de novo synthesis of protein(s). IPA Knowledge Base (Ingenuity) helped to identify proteins which could be part of this regulation. Among other proteins, we showed for the first time that GILZ (Glucocorticoid-induced leucine zipper; TSC22D3), hypothesised in the literature to decrease the production of CCL5, was up-regulated by VD. GILZ could therefore be responsible for a potential protective effect of VD on inflammation-induced expression of CCL2, 4 and 5.