Could Neutrophil Extracellular Traps Elucidate the Mysteries of Pathogenesis?
Received Date: Mar 28, 2014 / Accepted Date: Apr 26, 2014 / Published Date: Apr 28, 2014
Recently, NETosis emerged as a specific type of neutrophil death that is involved in innate immunity, and its products ‘’Neutrophil extracellular traps (NETs)’’ are now implicated as new candidates in a diversity of pathologic states. NET formation in contact to different pathogens or a variety of stimuli, is dependent on nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and involves the generation of reactive oxygen species (ROS). They consist of processed chromatin bound to granular and selected cytoplasmic proteins and act mainly via toll-like receptors (TLRs) signaling pathway. Pathogens trapped in NETs are killed through dual oxidative and non-oxidative mechanisms, even those so large that they cannot be phagocytosed. NETs participate in clot formation in blood vessels and might be cytotoxic to tumor cells. Conversely, different mechanisms were found to mediate the pathogenic role of NETs in different pathological states such as: vascular disorders; severe sepsis; autoimmune diseases; pulmonary disorders; pregnancy related disorders; cancer and otitis media. Thus, molecules that affect the balance of NET induction and destruction or attack the integrity of the NET structure like: NADPH inhibitors; deoxyribonuclease (DNase); blocking antibodies against histones or ROS scavengers can be of therapeutic value.
Keywords: Neutrophil extracellular traps; NEtosis; Pathogenesis; Histone-citrullination; Plasmacytoid dendretic cells; Autoimmune; Cancer
Citation: Amal Abd El hafez (2014) Could Neutrophil Extracellular Traps Elucidate the Mysteries of Pathogenesis?. J Clin Exp Pathol 4:174. Doi: 10.4172/2161-0681.1000174
Copyright: © 2014 Abd El hafez A. 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.