Reprogramming macrophages to an anti‐inflammatory phenotype by helminth antigens reduces murine atherosclerosis

• DOI: 10.1096/fj.13-235911
• Publication Date: 2013-09-17T04:07:56Z
• Authors: Ine M. J. Wolfs; J. Lauran Stöger; Pieter Goossens; Chantal Pöttgens; Marion J. J. Gijbels; Erwin Wijnands; Emiel P. C. Vorst; Patrick Gorp; Linda Beckers; David Engel; Erik A. L. Biessen; Georg Kraal; Irma Die; Marjo M. P. C. Do...; Menno P. J. Winther
• Keywords: Proinflammatory cytokine; Monocyte

Atherosclerosis is a lipid-driven inflammatory disease of the vessel wall, characterized by chronic activation macrophages.We investigated whether helminth-derived antigens [soluble egg (SEAs)] could modulate macrophage responses and protect against atherosclerosis in mice.In bone marrow-derived macrophages, SEAs induce anti-inflammatory typified high levels IL-10 reduced secretion proinflammatory mediators.In hyperlipidemic LDLR ؊/؊ mice, SEA treatment plaque size 44%, plaques were less advanced compared with PBS-injected littermate controls.The atheroprotective effect was found to be mainly independent cholesterol lowering T-lymphocyte but instead attributed diminished myeloid cell activation.SEAs circulating neutrophils Ly6C monocytes, macrophages showed production.In line observed systemic effects, atherosclerotic lesions SEA-treated mice intraplaque inflammation as markers [TNF-␣, monocyte chemotactic protein 1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), vascular (VCAM-1), CD68], neutrophil content, newly recruited macro-phages decreased.We show that protects development dampening responses.In future, helminthderived components may provide novel opportunities treat diseases, they diminish reduce immune cells.-