Upregulation of tumor necrosis factor-α expression by trans10-cis12 conjugated linoleic acid enhances phagocytosis of RAW macrophages via a peroxisome proliferator-activated receptor γ-dependent pathway

The aim of this study was to examine whether tumor necrosis factor (TNF)-α expression in the phagocytic activity of RAW macrophages by trans10-cis12 (10t-12c) conjugated linoleic acid (CLA) is associated with peroxisome proliferator-activated receptor γ (PPARγ) activation. 10t-12c CLA induced the TNF-α expression in RAW macrophages. Phagocytic activity of naive RAW macrophages was increased either by recombinant mouse (rm) TNF-α or by culture supernatant from 10t-12c CLA-treated RAW macrophages. This phagocytic activity was inhibited by addition of anti-rmTNF-α polyclonal antibody (pAb). 10t-12c CLA also increased the level of PPARγ protein and mRNA in RAW macrophages. When naive RAW macrophages were incubated with the culture supernatant from RAW macrophages treated with 10t-12c CLA plus GW 9662, a PPARγ antagonist, their phagocytic activity was significantly inhibited. In addition, GW 9662 antagonized the effect of 10t-12c CLA in stimulating TNF-α expression. These results suggest that 10t-12c CLA modulates the phagocytic activity of RAW macrophages by upregulating TNF-α expression via a PPARγ-dependent pathway.