Interleukin-10 inhibits intimal hyperplasia after angioplasty or stent implantation in hypercholesterolemic rabbits

Background-Intimal hyperplasia after stent implantation is the main cause o f in-stent restenosis. Activated monocytes play a key role in intimal growt h. The anti-inflammatory cytokine interleukin-10 (IL-10) is a potent monocy te deactivator, endogenously produced in the atherosclerotic plaque. We tes ted the hypothesis that exogenous IL-10 may limit postangioplasty intimal h yperplasia after balloon angioplasty or stenting, Methods and Results-Hypercholesterolemic rabbits were treated with recombin ant human IL-10 (rhuIL-10) for 3 days after balloon angioplasty or 28 days after stent implantation, High IL-10 serum levels and intense deactivation of circulating monocytic cells, assessed by inhibition of IL-1 beta release by lipopolysaccharide-stimulated whole blood, were detected for at least 8 hours after rhuIL-10 intravenous injection (ELISA). Morphometric analyses, performed 28 days after injury, indicated that rhuIL-10 reduced intimal gr owth by approximate to 50% after balloon angioplasty or stenting, resulting in more preserved lumen in stented arteries. Moreover rhuIL-10 reduced mac rophage infiltration by 67% and proliferative activity by 81% in the intima and the: media. No toxic effect was detected except minor changes in blood cell count, Conclusions-The anti-inflammatory cytokine rhuIL-10 reduces postinjury inti mal hyperplasia. The potent attenuation of in-stent intimal growth by rhuIL -10 and its favorable toxicity profile prevention of in-stent restenosis.