Macrophages mediate systemic tissue health after remote injury

Functions of tissue-resident macrophages in the steady state and after direct injury to the vital organs they inhabit are currently emerging. Yet, whether macrophages react to injury systemically and remotely, for instance how lung, liver or renal macrophages respond to myocardial infarction and stroke, remains obscure. Here we report that after myocardial infarction, stroke and peritonitis, macrophage populations expand in most distant organs through local cell proliferation and recruitment. Transcriptome profiling reveals a profound, system-wide response of macrophages to remote injury in all organs. This response is determined by the host organ rather than by injury type. We analyzed flow-sorted macrophages from lung, kidney, heart, liver and brain in the steady state, and after myocardial infarction, stroke and peritonitis induced by cecal ligation and puncture. At least three replicates were analyzed per organ and disease condition, for a total of 56 samples.