In agreement with our nutrigenomic results, a significant decreased adhesion of monocytes pre-exposed to MOF could be observed at the endothelial cells compared to control. The potential of grape seed extract to decrease adhesion of monocytes to HUVECs has been reported recently, however at concentrations ranging from 50 to 100 mg/ml. These concentrations are higher than the concentrations used in our study. Our results emphasize the capacity of grape seed– derived MOF to decrease the adhesion of immune cells to the vascular endothelium and potentially lower infiltration of these immune cells into the vascular wall, which is an initial step in atherosclerosis development. It has been reported that supplementation of the diet with catechin, a flavanol monomer present in MOF, results in lower atherosclerosis development in apolipoprotein E-deficient mice. It could be postulated that the regular consumption of MOF could decrease blood cell infiltration into the vasculature and potentially protect against atherosclerotic lesions in humans. Our bioinformatic data also revealed that over 30 differentially expressed genes are involved in different processes related to inflammation. The role of chronic inflammation in the promotion, initiation and development of chronic diseases, such as cancer, cardiovascular disease or osteoporosis has been described. In our study, among the differentially expressed genes involved in inflammatory processes is the gene coding for the proinflammatory cytokine IL2, of which the expression has been down-regulated by the MOF supplementation. Together with IL2, we also observed a decrease in the expression of a subunit of its receptor, the IL2RB gene. These inflammation-related genes, as well as some of the cell adhesion molecules, are regulated by the transcription factor NF-kB. Bioinformatic analyses of the nutrigenomic data identified several transcription factors potentially involved in the regulation of the expression of differentially expressed genes, among which is NF-kB. This suggests that NF-kB is a potential target by which MOF exert their anti-inflammatory effects in circulating blood cells. Interestingly, our nutrigenomic data also revealed an increase in the expression of the gene coding for NFKBIA, the endogenous inhibitor of NF-kB. A previous in vivo study in an atherosclerotic ApoE mouse model identified NF-kB as a major upstream regulator in leukocyte adhesion and transendothelial migration through the vascular endothelium. Moreover, NF-kB activity in peripheral blood mononuclear cells from smokers has been found to be significantly higher than in PBMCs from non-smokers. In order to corroborate a direct effect of MOF on NF-kB we performed NF-kB reporter gene studies in an inflammatory human monocyte/macrophage cell model. The experiments revealed a dose- and time-dependent repression of NF-kB luciferase expression in the presence of MOF.