Lack of Formyl-peptide Receptor 1 Mitigates Atherosclerosis in Hyperlipidemic Mice

Atherosclerosis is a chronic inflammatory disease of the arterial wall with hypercholesterolemia and inflammation representing two major pillars in its pathophysiology. A decade ago, studies unraveled how hypercholesterolemia influences inflammation and revealed that lipids orchestrate leukocyte homeostasis. Hypercholesterolemia-associated monocytosis and neutrophilia directly correlate with lesional leukocyte counts and lesion dimension in mice and with the incidence of cardiovascular events in humans.[1] [2] [3] In mice, for example, counts of circulating Ly6Chi inflammatory monocytes correlate with atherosclerotic lesion burden.[2] [4] Similarly, circulating neutrophil counts expand under hypercholesterolemia correlating with atherosclerotic plaque size and lesional neutrophil accumulation.[1] [5] [6] Analogous associations were already found in the 1970s, when it was noticed that peripheral leukocyte counts predict future cardiovascular events.[7] Very recently, these observations were extended by providing proof for the causality between high neutrophil counts and the risk for cardiovascular morbidity across several end points.[8] [9]