<![CDATA[Probetex, Inc. - Blog]]>Wed, 18 Oct 2017 22:15:16 -0700Weebly<![CDATA["Nothing but NET"]]>Sun, 18 Oct 2015 13:33:06 GMThttp://probetex.com/blog/1     Please excuse the basketball sports chiche, however Kumar et al scored a 3 pointer with their recent publication in JASN titled "Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN". J. Am. Soc. Nephrol. 26:2399-2413, 2015. See abstract...
Author Information: Santhosh V.R. Kumar,* Onkar P. Kulkarni,* Shrikant R. Mulay,* Murthy N. Darisipudi,*Simone Romoli,* Dana Thomasova,* Christina R. Scherbaum,* Bernd Hohenstein,† Christian Hugo,† Susanna Müller,‡ Helen Liapis,§ and Hans-Joachim Anders*
*Division of Nephrology, Department of Internal Medicine IV, Ludwig-Maximilians-University of Munich, Munich, Germany; †Division of Nephrology, Department of Internal Medicine III, Dresden University of Technology, Dresden, Germany; ‡Institute of Pathology, University of Munich, Munich, Germany; and §Department of Pathology and Immunology, School of Medicine, Washington University in Saint Louis, Saint Louis, Missouri

      Neutrophil extracellular traps (NETs) are large extracellular filamentous structures composed of granular proteins and modified nucleosomes that trap and kill
microorganisms providing a last resort to check infections by bacteria, fungi, parasites, and viruses. NETs are produced through a process of neutrophil cell death referred to as “NETosis” where processed chromatin binds to granular proteins that are extruded into the extracellular environment. A variety of stimuli induce NETosis including components of microorganisms, reactive oxygen species, immune complexes, etc. NETs can also kill mammalian cells and in various inflammatory conditions may cause collateral pathological consequences as is observed in Lupus, Anti-Neutrophil Cytoplasmic Antibody (ANCA) vasculitis and other autoimmune diseases. The mechanisms of this phenomenon are poorly understood and continue to be the subject of considerable investigation.  

       In their seminal study, Kumar et al. show that NET formation plays an important local cytotoxic component of severe anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). NETs were shown to kill glomerular endothelial cells, podocytes and parietal epithelial cells in vitro, an effect that could be neutralized by histone-neutralizing agents. Similarly, blocking NET formation in vivo significantly reduced glomerular vasculitis induced by anti-GBM antiserum and characterized by vascular necrosis, podocytes loss albuminuria, cytokine induction, leukocyte recruitment and crescent formation. This study establishes a role for NETs in anti-GBM GN and emphasizes the importance of extracellular histones as cytototoxic agents and important therapeutic targets in immune-mediated vasculitis.

      Probetex offers a variety of nephrotoxic antibodies and services for the investigation of basic mechanisms and therapeutic approaches to immune-mediated renal disease.
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Anti-GBM Nephritis