A Role for Palmitoleate in Regulating Macrophage Activation

Abstract

Increased macrophage proinflammatory activation contributes to atherosclerotic problems. We investigated the effects of palmitoleate treatment on the inflammatory status of bone marrow‐derived macrophages (BMDM). After differentiation, wild‐type BMDM were treated with palmitoleate (50 μM) for 48 h in the presence of lipopolysaccharides (LPS, 100 ng/ml) for the last 30 min to stimulate macrophage proinflammatory signaling or interleukin‐4 (IL‐4, 10 ng/ml) for 48 h to inhibit macrophage proinflammatory activation. LPS stimulation caused an increase in the phosphorylation of JNK1/2 and NF‐κB p65 in BMDM. This stimulatory effect of LPS was partially blunted by treatment with palmitoleate. On the other hand, IL‐4 displayed a weak effect on decreasing the phosphorylation of JNK1/2 and NF‐κB p65 in BMDM. However, in palmitoleate‐treated BMDM, the inhibitory effect of IL‐4 was much more potent, evidenced by the fact that the combined treatment with IL‐4 and palmitoleate nearly abolished the phosphorylation of JNK1/2 and significantly decreased the phosphorylation of NF‐κB p65. Together, these data suggest that palmitoleate is anti‐inflammatory bioactive lipid which may be useful for prevention of cardiovascular disease.Grant Funding Source: American Diabetes Association, American Heart Association