Abstract
Histones are positively charged nuclear proteins that facilitate packaging of DNA into nucleosomes common to all eukaryotic cells. Upon cell injury or cell signalling processes, histones are released passively through cell necrosis or actively from immune cells as part of extracellular traps. Extracellular histones function as microbicidal proteins and are pro‐thrombotic, limiting spread of infection or isolating areas of injury to allow for immune cell infiltration, clearance of infection and initiation of tissue regeneration and repair. Histone toxicity, however, is not specific to microbes and contributes to tissue and end‐organ injury, which in cases of systemic inflammation may lead to organ failure and death. This review details the processes of histones release in acute inflammation, the mechanisms of histone‐related tissue toxicity and current and future strategies for therapy targeting histones in acute inflammatory diseases.
Highlights
Histones were first described by Albrecht Kossel in 1884 as histidine‐rich peptones derived from the nuclear component of avian red blood cells[1]; he was awarded the Nobel Prize in Physiology or Medicine for this and other work on the nucleus of cells in 1910
Controlled histone degradation has been described in neutrophils leading to chromatin decondensation and release of genomic DNA laced with granular proteins as neutrophil extracellular traps (NETs).[6,7]
Histones and histone fragments are parts of an ancient antimicrobial mechanism conserved throughout eukaryotic species
Summary
Histones were first described by Albrecht Kossel in 1884 as histidine‐rich peptones derived from the nuclear component of avian red blood cells[1]; he was awarded the Nobel Prize in Physiology or Medicine for this and other work on the nucleus of cells in 1910. Controlled histone degradation has been described in neutrophils leading to chromatin decondensation and release of genomic DNA laced with granular proteins as neutrophil extracellular traps (NETs).[6,7] These meshwork‐like structures promote intravascular thrombosis,[8] limit spread of microorganisms, encourage cancer metastasis[9] and cause direct injury to adjacent cells.[10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
