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Is Histone a Solitary Vile Sepsis-Inducing Agent or Just "a Member of the Gang"?
Isaac Ginsburg1*, Erez Koren1,2 Uriel Trahtemberg3 and Peter Vernon van Heerden3*
1Hadassah Faculty of Dental Medicine, Institute for Dental Sciences the Hebrew University, Jerusalem, Israel
2Teva Pharmaceutical Industries Ltd., Kfar Saba, Israel
3General Intensive Care Unit, Hadassah University Hospital, Jerusalem, Israel
- *Corresponding Authors:
- Isaac Ginsburg
Hadassah Faculty of Dental Medicine
Institute for Dental Sciences the Hebrew University, Jerusalem, Israel
E-mail: Ginsburg@mail.huji.ac.il - Peter Vernon van Heerden
General Intensive Care Unit
Hadassah University Hospital, Jerusalem, Israel
E-mail: Vernon@hadassah.org.il
Received date: August 02, 2017; Accepted date: August 08, 2017; Published date: August 12, 2017
Citation: Ginsburg I, Koren E, Trahtemberg U, van Heerden PV (2017) Is Histone a Solitary Vile Sepsis-Inducing Agent or Just "a Member of the Gang"?. J Infect Dis Ther 5:329. doi: 10.4172/2332-0877.1000329
Copyright: © 2017 Isaac G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
In this communication we argue that it is improbable that the main cause of death in sepsis is that, upon release of extracellular traps from neutrophils adhering to endothelial cells, highly cationic toxic histones uniquely cause endothelial dysregulation, organ failure and death. Activation of neutrophils is always accompanied by a plethora of pro-inflammatory agents, which may act in synergy with histones to injure cells. Furthermore, many recent articles have shown a steep rise of circulating histones in many clinical disorders unrelated to sepsis. We argue therefore that histones do not act as unique alarmins with an outsized role, but are probably another marker of cell damage.
