Sepsis and septic shock are among the leading causes of death in intensive care units worldwide. Numerous studies on their pathophysiology have revealed an imbalance in the inflammatory network leading to tissue damage, organ failure, and ultimately, death. Cytokines are important pleiotropic regulators of the immune response, which have a crucial role in the complex pathophysiology underlying sepsis. They have both pro- and anti-inflammatory functions and are capable of coordinating effective defense mechanisms against invading pathogens. On the other hand, cytokines may dysregulate the immune response and promote tissue-damaging inflammation. In this review, we address the current knowledge of the actions of pro- and anti-inflammatory cytokines in sepsis pathophysiology as well as how these cytokines and other important immunomodulating agents may be therapeutically targeted to improve the clinical outcome of sepsis.

/pdf/cytokines-in-sepsis-potent-immunoregulators-and-potential-1olx7frrhj.pdf

Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets—An Updated View

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jth.13911

Inflammation and thrombosis: roles of neutrophils, platelets and endothelial cells and their interactions in thrombus formation during sepsis

The endothelium provides an essential and selective membrane barrier that regulates the movement of water, solutes, gases, macromolecules and the cellular elements of the blood from the tissue compartment in health and disease. Its structure and continuous function is essential for life for all vertebrate organisms. Recent evidence indicates that the endothelial surface does not have a passive role in systemic inflammatory states such as septic shock. In fact, endothelial cells are in dynamic equilibrium with a myriad of inflammatory mediators and elements of the innate immune and coagulation systems to orchestrate the host response in sepsis. The barrier function of the endothelial surface is almost uniformly impaired in septic shock, and it is likely that this contributes to adverse outcomes. In this review, we will highlight recent advances in the understanding of the signalling events that regulate endothelial function and molecular events that induce endothelial dysfunction in sepsis. Endothelial barrier repair strategies as a treatment for sepsis include modulation of C5a, high-mobility group box 1 and VEGF receptor 2; stimulation of angiopoietin-1, sphingosine 1 phosphate receptor 1 and Slit; and a number of other innovative approaches.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/joim.12331

Endothelial barrier dysfunction in septic shock

Freeze tolerance is an amazing winter survival strategy used by various amphibians and reptiles living in seasonally cold environments. These animals may spend weeks or months with up to ∼65% of th...

Molecular Physiology of Freeze Tolerance in Vertebrates.

Sepsis-induced myocardial dysfunction is a common complication in septic patients and is associated with increased mortality. In the clinical setting, it was once believed that myocardial dysfunction was not a major pathological process in the septic patients, at least in part, due to the unavailability of suitable clinical markers to assess intrinsic myocardial function during sepsis. Although sepsis-induced myocardial dysfunction has been studied in clinical and basic research for more than 30 years, its pathophysiology is not completely understood, and no specific therapies for this disorder exist. The purpose of this review is to summarize our current knowledge of sepsis-induced myocardial dysfunction with a special focus on pathogenesis and clinical characteristics.

/pdf/pathophysiology-of-sepsis-induced-myocardial-dysfunction-2dipi41wty.pdf

Pathophysiology of sepsis-induced myocardial dysfunction

I. Alwayn, Halifax D.K. Bartsch, Marburg C. Bassi, Verona W.O. Bechstein, Frankfurt am Main J.A. Bradley, Cambridge M. Cikirikcioglu, Geneva P.-A. Clavien, Zurich C. Eipel, Rostock R.W.F. de Bruin, Rotterdam H. Friess, Munich S. Fichtner-Feigl, Regensburg G. Galata, London D.J. Gouma, Amsterdam J.K. Habermann, Lübeck M. Heberer, Basel W.R. Jarnagin, New York, NY J.C. Kalff , Bonn M.W. Laschke, Homburg/Saar H.-A. Lehr, Lausanne C.M. Malata, Cambridge T. Minor, Bonn M. Morino, Torino J. Pirenne, Leuven R. Schramm, Munich L. Steinstraesser, Bochum T.M. van Gulik, Amsterdam M.A. Venermo, Helsinki D.C. Winter, Dublin Y. Yamamoto, Akita Clinical and Experimental Surgery

Contents Vol. 48, 2012

The concept that sepsis is the result of an uncontrolled inflammatory response of the host’s innate immune system towards invading pathogens has recently been challenged. Evidence is accumulating that

/pdf/damage-and-pathogen-associated-molecular-patterns-and-8vdu6m8p1y.pdf

Damage- and pathogen-associated molecular patterns and alarmins: keys to sepsis?

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Contents Vol. 48, 2012

Damage- and pathogen-associated molecular patterns and alarmins: keys to sepsis?