ABCA1 protein enhances Toll-like receptor 4 (TLR4)-stimulated interleukin-10 (IL-10) secretion through protein kinase A (PKA) activation.

摘要: Nonresolving inflammatory response from macrophages is a major characteristic of atherosclerosis. Macrophage ABCA1 has been previously shown to suppress the secretion proinflammatory cytokine. In present study, we demonstrate that also promotes IL-10, an anti-inflammatory cytokine critical for inflammation resolution. ABCA1+/+ bone marrow-derived secrete more IL-10 but less cytokines than ABCA1−/− macrophages, similar alternatively activated (M2) macrophages. We evidence activates PKA and this elevated activity contributes M2-like Furthermore, cholesterol lowering by statins, methyl-β-cyclodextrin, or filipin and, consequently, transforms toward phenotype. Conversely, enrichment suppresses M1-like response. As primary function removal, our results suggest regulating cholesterol. Indeed, forced in ABCA1-expressing activation elicits Collectively, these findings reveal novel protective process ABCA1-activated They extra-hepatic tissues statins as anti-inflammation strategy.