Figure 6

Potential atheroprotective mechanism of CLA on the macrophage/foam cell axis. (a) Th-1 cytokine environment primes M-CSF-triggered monocyte differentiation towards an MΦ1 macrophage pro-inflammatory phenotype. (b) Th-2 cytokine environment primes M-CSF-triggered monocyte differentiation towards an MΦ2 macrophage anti-inflammatory phenotype. (c) CLA action primes M-CSF-triggered monocyte differentiation towards an MΦ2-type macrophage. (d) In the presence of high levels of lipids in the extracellular matrix, CLA induces a dual mechanism PPARγ/LXRα-mediated (i-ii), by increasing CD36 levels (iii), allowing lipids to enter the cell (iv), and secondly, promoting cholesterol efflux, by increasing ABCA-1 mRNA expression (v), thus preventing lipid engulfment of the cell (vi), and the consequent foam cell formation. Moreover, CLA inhibits the secretion of pro-inflammatory cytokines (vii).