Obesity is associated with a chronic low-grade inflammatory state. In fact, fat mass expansion is linked to an oversecretion of inflammatory markers which originate predominantly from macrophage accumulation in the adipose tissue (AT). The recruitment of macrophages in human AT is not completely understood. Therefore, this paper tested the hypothesis that a precise chemokine, chemokine ligand (CCL) 5, may participate with other chemokines, such as CCL2, in the recruitment of monocytes and the survival of macrophages in human white AT. An increase in CCL5 secretion and gene expression was observed in AT of both obese men and women. Moreover, secretion levels of CCL5 were higher in obese visceral adipose depots compared to that in subcutaneous AT. CCL5 gene expression was strongly correlated with T-lymphocyte markers in visceral AT. Another finding was that CCL5 triggered adhesion and transmigration of blood monocytes to/through endothelial cells of human AT. In vitro studies clearly demonstrated the antiapoptotic action of CCL5 on macrophages which appeared to be mediated via the Erk/Akt pathways. These findings support a role for CCL5 in the inflammation of obese white AT through the recruitment of blood monocytes and its antiapoptotic effect on AT macrophages. It is suggested that CCL5 receptors may represent a potential target for controlling low-grade inflammation in obesity.
Documentation centre