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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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Journal ArticleDOI

Sepsis: Current Dogma and New Perspectives

TL;DR: It is argued that it is time to delineate novel immunometabolic and neurophysiological mechanisms underlying the altered cellular bioenergetics and failure of epithelial and endothelial barriers that produce organ dysfunction and death.
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The immune system's role in sepsis progression, resolution, and long‐term outcome

TL;DR: Efforts are focused on more clearly defining and effectively reversing the persistent immune cell dysfunction associated with long‐term sepsis mortality, which alters the innate and adaptive immune responses for sustained periods of time after clinical recovery.
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Sepsis-induced immune dysfunction: can immune therapies reduce mortality?

TL;DR: These efforts are focused on defining and reversing the persistent immune cell dysfunction that is associated with mortality long after the acute events of sepsis have resolved.
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Complement in Immune and Inflammatory Disorders: Pathophysiological Mechanisms

TL;DR: This review provides an update about the functional and collaborative capabilities of complement, highlights major disease areas with known complement contribution, and indicates the potential for complement as a focal point in immunomodulatory strategies for treating inflammatory diseases.
References
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Cecal ligation and puncture: the gold standard model for polymicrobial sepsis?

TL;DR: It is demonstrated that experimental sepsis models do not completely mimic human sepsi, and several therapies proposed on the basis of promising results obtained by CLP could not be translated to the clinic.
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The sepsis seesaw: tilting toward immunosuppression.

TL;DR: Recent human studies bolstering the notion that immunosuppression is also a major contributor to the disease are assessed.
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Endogenous ligands of TLR2 and TLR4: agonists or assistants?

TL;DR: The evidence supporting the intrinsic TLR‐stimulating capacity of each of these proposed endogenous ligands is summarized with a particular emphasis on the measures taken to exclude contaminating LPS and lipopeptides from experimental systems.
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Animal models of sepsis and sepsis-induced kidney injury

TL;DR: A bedside- to-bench-to-bedside approach that has resulted in improved animal models for the study of sepsis - a complex disease for which preventive and therapeutic strategies are unfortunately lacking.
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Antidiabetic actions of a non-agonist PPARγ ligand blocking Cdk5-mediated phosphorylation

TL;DR: Novel synthetic compounds are described that have a unique mode of binding to PPARγ, completely lack classical transcriptional agonism and block the Cdk5-mediated phosphorylation in cultured adipocytes and in insulin-resistant mice, and one such compound, SR1664, has potent antidiabetic activity while not causing the fluid retention and weight gain that are serious side effects of many of the PParγ drugs.
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