Abstract:

 In this communication we argue that it is improbable that the main cause of death in sepsis is that, upon releaseof extracellular traps from neutrophils adhering to endothelial cells, highly cationic toxic histones uniquely causeendothelial dysregulation, organ failure and death. Activation of neutrophils is always accompanied by a plethora ofpro-inflammatory agents, which may act in synergy with histones to injure cells. Furthermore, many recent articleshave shown a steep rise of circulating histones in many clinical disorders unrelated to sepsis. We argue thereforethat histones do not act as unique alarmins with an outsized role, but are probably another marker of cell damage.