About this Research Topic
Irrespectively of infectious or sterile origin, inflammation affects the endothelial structure and its permeability, resulting in the release of endogenous cell injury–associated molecules (damage-associated molecular patterns, DAMPs). The release of DAMPs or pathogen-associated molecular patterns (PAMPs) in turn leads to activation of receptors mediating the fatal amplification of pro-inflammatory cascades. Moreover, other mechanisms such as formation of neutrophil extracellular traps (NETs) contribute to amplified inflammation and may lead in excess to life-threatening organ dysfunctions like encephalopathy, acute kidney injury, respiratory failure, and cardiomyopathy. This series of events in the immune response contributes to further functional loss in organs not involved in the primary focus. As a result an avalanche-like development of sequential organ dysfunction is observed at the bedside being incalculable in its result. A deeper understanding on the body’s response to inflammatory stimuli may add to the progress in specific interventions to protect us against our own overwhelming defense mechanisms.
In this Research Topic, hosted by Frontiers in Immunology, we aim to shed light on mediators and the interactive crosstalk between organs in both sterile and infectious inflammation. This may include basic research and corresponding animal and human research. We will highlight key mechanisms of inflammation research to further discussion on the development of therapeutic attempts to limit excess inflammatory actions.
Keywords: sepsis, organ dysfunction, molecular mechanisms, organ crosstalk