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CitH3: An Early Detection of Sepsis Following Hemorrhagic Shock? A View

Volume 3 - Issue 2

Manoj Kumar*1, Sanjeev Bhoi2 and Sagar Galwankar3

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    • 1Department of Microbiology, Al-Falah School of Medical Science and Research Centre, India
    • 2Department of Emergency Medicine, JPNATC, AIIMS, India
    • 3Faculty of Emergency Medicine & Global Health, University of South Florida, USA

    *Corresponding author: Manoj Kumar, Tutor, Department of Microbiology, Al-Falah School of Medical Science and Research Centre, Dhauj, Faridabad, Haryana-121004, India

Received: March 05, 2018;   Published: March 20, 2018

DOI: 10.26717/BJSTR.2018.03.000871

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Hemorrhagic shock (HS) induces inflammatory cytokines leads to susceptible to infection, sepsis and multi-organ failure [1]. Sepsis is remaining leading cause of death within intensive care unit after trauma. Mortality rates are approximately ∼20-30%. [2]. Ginsburg, Reported that the main cause of death in sepsis is the release from neutrophil nets of nuclear histone, highly toxic to endothelial cells and that these polycations are major and unique virulence factors Ginsburg et al. [3]. Neutrophils play an important role as the first line of defence of the immune system. In addition, one role of neutrophils, called neutrophil extracellular traps (NETs), has been discovered recently [3]. NETs are fibrous structures that are released extracellularly from activated neutrophils in response to infection and also the sterile inflammatory process. Modification by citrullination of histone H3 (CitH3) is thought to be involved in the in vitro formation of NETs [4,5].

Abbrevations: HS: Hemorrhagic Shock; NETs: Neutrophil Extracellular Traps; CitH3: Citrullination of Histone H3; PTM: Post-Translational Modification; PAD: Peptidylarginine Deiminase; ETs: Immune Cells Extracellular Traps

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