Targeting Cytokines, Pathogen-Associated Molecular Patterns, and Damage-Associated Molecular Patterns in Sepsis via Blood Purification.
Kazuhiro Moriyama,Osamu Nishida +1 more
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TLDR
In this review, recent advances in knowledge regarding the role of lipopolysaccharides, cytokines, DAMPs, and neutrophils in the pathogenesis of sepsis are summarized and the potential of blood purification, especially the adsorption technology, for removing immune cells and molecular mediators, thereby serving as a therapeutic strategy againstsepsis is discussed.Abstract:
Sepsis is characterized by a dysregulated immune response to infections that causes life-threatening organ dysfunction and even death. When infections occur, bacterial cell wall components (endotoxin or lipopolysaccharide), known as pathogen-associated molecular patterns, bind to pattern recognition receptors, such as toll-like receptors, to initiate an inflammatory response for pathogen elimination. However, strong activation of the immune system leads to cellular dysfunction and ultimately organ failure. Damage-associated molecular patterns (DAMPs), which are released by injured host cells, are well-recognized triggers that result in the elevation of inflammatory cytokine levels. A cytokine storm is thus amplified and sustained in this vicious cycle. Interestingly, during sepsis, neutrophils transition from powerful antimicrobial protectors into dangerous mediators of tissue injury and organ dysfunction. Thus, the concept of blood purification has evolved to include inflammatory cells and mediators. In this review, we summarize recent advances in knowledge regarding the role of lipopolysaccharides, cytokines, DAMPs, and neutrophils in the pathogenesis of sepsis. Additionally, we discuss the potential of blood purification, especially the adsorption technology, for removing immune cells and molecular mediators, thereby serving as a therapeutic strategy against sepsis. Finally, we describe the concept of our immune-modulating blood purification system.read more
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References
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The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)
Mervyn Singer,Clifford S. Deutschman,Christopher W. Seymour,Manu Shankar-Hari,Djillali Annane,Michael Bauer,Rinaldo Bellomo,Gordon R. Bernard,Jean-Daniel Chiche,Craig M. Coopersmith,Richard S. Hotchkiss,Mitchell M. Levy,John C. Marshall,Greg S. Martin,Steven M. Opal,Gordon D. Rubenfeld,Gordon D. Rubenfeld,Tom van der Poll,Jean Louis Vincent,Derek C. Angus +19 more
TL;DR: The task force concluded the term severe sepsis was redundant and updated definitions and clinical criteria should replace previous definitions, offer greater consistency for epidemiologic studies and clinical trials, and facilitate earlier recognition and more timely management of patients with sepsi or at risk of developing sepsic shock.
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Neutrophil extracellular traps kill bacteria
Volker Brinkmann,Ulrike Reichard,Christian Goosmann,Beatrix Fauler,Yvonne Uhlemann,David S. Weiss,Yvette Weinrauch,Yvette Weinrauch,Arturo Zychlinsky +8 more
TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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The immunopathogenesis of sepsis.
TL;DR: Because of the high mortality of sepsis in the face of standard treatment, many efforts have been made to improve understanding of the dysregulation of the host response in sepsi, and much has been learnt of the basic principles governing bacterial–host interactions.
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The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)
TL;DR: The reported incidence of sepsis is increasing, likely reflecting aging populations with more comorbidities, greater recognition, and, in some countries, reimbursement-favorable coding.
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Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death
TL;DR: The discovery of caspase-11/4/5 function in sensing intracellular lipopolysaccharide expands the spectrum of pyroptosis mediators and also reveals that pyroPTosis is not cell type specific.