title: Fighting against the dark side of neutrophil extracellular traps in disease:  manoeuvres for host protection.
abstract: OBJECTIVE
  This review presents a concise summary of the role of neutrophil extracellular traps (NET) in several pathological situations associated with adverse effects of NET. Different strategies are indicated to dampen the unfavourable consequences of NET formation and function.
  
  
  RESULTS
  A major extracellular antimicrobial mechanism of neutrophils is induced by formation of NET, in which the microorganisms are trapped within the released chromatin from neutrophils and killed by highly concentrated, NET-entangled antimicrobial proteins. In recent years, exaggerated NET formation and the subsequent complications for the host organism have been reported in several pathological conditions. It has been shown that interfering with NET structure and/or components either via DNase to disrupt the DNA backbone of NET or via antihistone approaches to target the major proteins in NET can diminish the pathological symptoms in such diseases.
  
  
  CONCLUSIONS
  On the basis of the type of the disease and its severity as well as the outcome of NET generation, different therapeutic strategies may be considered to dampen the inauspicious consequences of exaggerated NET formation and function. Applying combinations of compounds that aim to decrease the adverse activity of DNA and NET-associated proteins/enzymes may increase the efficiency of treatment.
authors.affiliation: Department of Biochemistry, School of Medicine, Justus-Liebig-University, Giessen, Germany.
authors.forename: Mona
authors.initials: M
authors.lastname: Saffarzadeh
authors.forename: Klaus T
authors.initials: KT
authors.lastname: Preissner
mesh_terms: D055371:Acute Lung Injury / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016923:Cell Death / Q000502:physiology; D003550:Cystic Fibrosis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007239:Infections / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D013927:Thrombosis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology