About this Research Topic
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.
Keywords: trauma, sepsis, inflammation, organ injury, DAMPs, PAMPs, glycocalyx
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