Eriodictyol decreases very late antigen-4 (VLA-4) expression, cellular adhesion, and migration through an NFκB-dependent pathway in monocytes

Abstract

Very late antigen-4 (VLA-4)-mediated monocyte adhesion and transendothelial migration are important events during immune surveillance and in the pathogenesis of inflammatory diseases, such as atherosclerosis. Under physiological conditions, circulating monocytes that are in various states of maturation enter tissue microenvironments and participate in immune responses by interacting with other leukocytes. The effects and regulatory mechanisms of eriodictyol on VLA-4 expression, cell adhesion, and migration in U937 cells were investigated. Eriodictyol lowered VLA-4 expression in a dose- and time-dependent manner in U937 cells. Moreover, VLA-4- and vascular adhesion molecular-1 (VCAM-1)-mediated adhesion and migration were decreased by eriodictyol. Upon treatment with eriodictyol, NF-κB translocated to the nucleus; the NF-κB inhibitor JSH-23 inhibited this translocation and prevented the decrease of VLA-4 expression by eriodictyol. Thus, eriodictyol regulates immune responses by modulating VLA-4 expression, cellular migration, and VLA-4-mediated adhesion in monocytes – evidence that eriodictyol regulates adhesion molecules during immune responses.