@article {21091,
	title = {Tissue damage in post infectious sequelae is caused by a synergism between microbial and neutrophils-derived agonists: a concern for a disregard for already published data},
	journal = {Journal of Emerging and Rare Diseases},
	volume = {1},
	number = {1},
	year = {2017},
	pages = {1-3},
	abstract = {Post infectious sequelae such as sepsis and septic shock are poorly understood and annually take the lives of millions over the world. Severe microbial infections caused by Gram Positive and Gram Negative bacteria and by fungi are the main causes, which are aggravated by the rapid development of antibiotic resistance. It is unfortunate that today all the clinical trials of sepsis which tested the efficacy of single antagonists failed. Sepsis was recently redefined as a synergistic multifactorial episode where no unique alarmin had been identified, which if inhibited could control the deleterious biochemical and immune immunological events characteristic of sepsis. An apparent {\textquotedblleft}breakthrough {\textquotedblleft}in our understanding of sepsis pathogenicity was published in 2009 in Nature Medicine arguing that the main cause of mortality in sepsis is the release from neutrophils (PMNs) nets of highly toxic nuclear histone. This caused endothelial cell dysregulation leading to organ failure. However, this concept downplays the concept that concomitantly with the activation of PMNs, a plethora of additional proinflammatory agents is also released. These can act in synergy with histone to injure cells. Furthermore, since many additional clinical disorders not related to sepsis also reported high levels of circulating histones, this toxic agent may be considered just another marker of cell damage. The failure to treat sepsis by the administration of only single antagonists should be replaced by cocktails of appropriate anti inflammatory agents.},
	url = {https://www.boffinaccess.com/open-access-journals/journal-of-emerging-and-rare-diseases/jer-1-101.pdf},
	author = {Ginsburg, I. and Koren, E. and Van Heerden, V.}
}
