Allicin inhibits SDF‐1α‐induced T cell interactions with fibronectin and endothelial cells by down‐regulating cytoskeleton rearrangement, Pyk‐2 phosphorylation and VLA‐4 expression

Summary Allicin, a major ingredient of fresh garlic extract that is produced during the crushing of garlic cloves, exerts various beneficial biological effects, including a broad spectrum of antimicrobial activity, antihyperlipidaemic and antihypertensive effects. However, how allicin affects the immune system is less well known, and its effect on human T cells has never been studied. Here, we examined the in‐vitro effects of allicin on the functioning of T cells related to their entry to inflamed extravascular sites. We found that allicin (20–100 µm) inhibits the SDF‐1α (CXCL12)‐induced T cell migration through fibronectin (FN), and that this inhibition is mediated by the down‐regulation of (i) the reorganization of cortical actin and the subsequent T cell polarization, and (ii) T cell adhesion to FN. Moreover, allicin also inhibited T cell adhesion to endothelial cells and transendothelial migration. The mechanisms underlying these inhibitory effects of allicin are associated with its ability to down‐regulate the phosphorylation of Pyk2, an intracellular member of the focal adhesion kinases, and to reduce the expression of the VCAM‐1‐ and FN‐specific α4β1‐integrin (VLA‐4). The ability of allicin to down‐regulate these chemokine‐induced and VLA‐4‐mediated T cell functions explains its beneficial biological effects in processes where T cells play an important role and suggests that allicin may be used therapeutically with chronic inflammatory diseases.