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Open AccessJournal ArticleDOI

The inflammatory response in sepsis.

Markus Bosmann, +1 more
- 01 Mar 2013 - 
- Vol. 34, Iss: 3, pp 129-136
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TLDR
Recent insights into the signaling pathways in immune and phagocytic cells that underlie sepsis and SIRS are discussed and how these might be targeted for therapeutic interventions to reverse or attenuate pathways that lead to lethality during sepsi are considered.
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This article is published in Trends in Immunology.The article was published on 2013-03-01 and is currently open access. It has received 382 citations till now. The article focuses on the topics: Systemic inflammatory response syndrome & Septic shock.

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Citations
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Leukotriene B4-mediated sterile inflammation promotes susceptibility to sepsis in a mouse model of type 1 diabetes

TL;DR: In this article, the authors hypothesized that low insulin concentrations in Type 1 diabetes mellitus (T1DM) trigger the enzyme 5-lipoxygenase (5-LO) to produce the lipid mediator leukotriene B4 (LTB4), which triggers systemic inflammation that may increase susceptibility to polymicrobial sepsis.
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Ubiquitylation of MFHAS1 by the ubiquitin ligase praja2 promotes M1 macrophage polarization by activating JNK and p38 pathways.

TL;DR: Results indicate that MFHAS1 ubiquitylation by praja2 positively regulates TLR2-mediated JNK/p38 pathway and promotes M1 macrophage polarization, M2 to M1macrophage transformation and inflammation.
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Antimicrobial effects of mesenchymal stem cells primed by modified LPS on bacterial clearance in sepsis.

TL;DR: Preconditioning was established as a strategy to increase the cells’ efficiency in order to revive infectious diseases, including sepsis, through stem cell transplantation.
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Nanotherapies for sepsis by regulating inflammatory signals and reactive oxygen and nitrogen species: New insight for treating COVID-19.

TL;DR: In this article, the authors discuss the pathogenesis of sepsis related to inflammation and the overproduction of reactive oxygen and nitrogen species (RONS), which activate pathogen-associated molecular pattern (PAMP)-pattern recognition receptor (PRR) and damage-associated molecule pattern (DAMP)-PRR signaling pathways.
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Glycyrrhizin Protects Rats from Sepsis by Blocking HMGB1 Signaling.

TL;DR: GL may protect rats against sepsis by blocking the interaction of HMGB1 with cell surface receptors and HMGB2-mediated inflammatory responses and the downstream MAPKs/NF-κB signaling pathway.
References
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The Epidemiology of Sepsis in the United States from 1979 through 2000

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TL;DR: Progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors, and on developing novel therapeutics that can facilitate and enhance lung repair.
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Immunodesign of experimental sepsis by cecal ligation and puncture.

TL;DR: Standardized procedures for inducing sepsis in mice and rats are defined by applying defined severity grades of sepsi through modulation of the position of cecal ligation.
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Immunosuppression in patients who die of sepsis and multiple organ failure.

TL;DR: Patients who die in the ICU following sepsis compared with patients who die of nonsepsis etiologies have biochemical, flow cytometric, and immunohistochemical findings consistent with immunosuppression, and targeted immune-enhancing therapy may be a valid approach in selected patients with sepsi.
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