(261) Reduction of cytokine levels in human macrophages over-expressing CD163

Abstract

Extended levels of inflammation after major surgeries contribute to the development of chronic pain. In normal wound healing, inflammatory macrophages (M1 phenotype) transition to antiinflammatory macrophages (M2 phenotype). CD163 is highly expressed in M2 macrophages, whereby CD163 seems to play a major role in the induction of M2 macrophages. We hypothesize that the genetic overexpression of CD163 in M1 macrophages will induce an earlier and efficient M2 phenotypic shift. THP-1 macrophages were stimulated with lipopolysaccharide (LPS, 1μg/mL) or interleukin-6 (IL-6, 50ng/mL) in the presence or absence of either CD163 plasmid or an empty plasmid, both conjugated with the nanoparticle polyethylenimine grafted with a mannose receptor ligand (mPEI).