Translational Insights into Mechanisms and Therapy of Organ Dysfunction in Sepsis and Trauma

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Editorial

25 September 2020

Editorial: Translational Insights Into Mechanisms and Therapy of Organ Dysfunction in Sepsis and Trauma

Peter Radermacher

,

Timothy R. Billiar

,

Pietro Ghezzi

,

Lukas Martin

and

Christoph Thiemermann

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6 citations

Editors

5

Lukas Martin

University Hospital RWTH Aachen

Christoph Thiemermann

Queen Mary University of London

Pietro Ghezzi

Brighton and Sussex Medical School

Peter Radermacher

University of Ulm

Timothy Robert Billiar

University of Pittsburgh

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Life-threatening organ dysfunction/failure in critically ill patients suffering from sepsis or trauma is caused by a dysregulated host response to infection and/or inflammation. Despite significant advances in our understanding of some of the key signaling pathways involved in the excessive inflammation associated with sepsis/trauma, the translation of our current understanding of the underlying pathophysiology into organ-protective therapeutic strategies is still very limited. Current therapeutic approaches, hence, continue to rely on source control, antibiotics and supportive care, and particularly early goal-directed therapy.

The organ dysfunction/failure associated with trauma and/or sepsis is associated with excessive systemic inflammation, secondary to extensive tissue damage and ischemia reperfusion injury. The endothelial glycocalyx is one of the earliest sites involved in triggering the potentially overwhelming pro-inflammatory response induced. Alterations to its structure affect (i) endothelial permeability and (ii) the secretion and activation of sheddases, leading to the release of degradation products of the endothelial glycocalyx (endogenous damage/danger associated molecular patterns; DAMPs). In addition to pathogen-associated molecular patterns (PAMPs) released from pathogens, DAMPs trigger and amplify the systemic inflammation present in patients suffering from many forms of critical illness. Thus, the injury of the glycocalyx and the consecutive release of DAMPs jointly contribute to and drive a potentially excessive, local and systemic inflammation which lead to organ injury/dysfunction including acute kidney injury, respiratory failure and cardiomyopathy, to name but a few.

In this Research Topic, we aim to shed new light on the molecular mechanisms involved in inflammation in critical illness with a focus on preclinical and translational studies targeting new organ-protective, therapeutic strategies in sepsis and trauma.

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Editors

Lukas Martin

University Hospital RWTH Aachen

Christoph Thiemermann

Queen Mary University of London

Pietro Ghezzi

Brighton and Sussex Medical School

Peter Radermacher

University of Ulm

Timothy Robert Billiar

University of Pittsburgh

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Published In

Frontiers in Immunology

Inflammation

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