Year: 2018
Type: editorial
Abstract: Sepsis is a syndrome of acute organ dysfunction caused by the physiologic and pathophysiologic response to infection [1–3]. Although the specific clinical definition of sepsis continues to evolve, the entity has been recognised in some form or other for thousands of years. Yet, distressingly, over 30 million cases of sepsis still occur globally each year, resulting in over 5 million deaths, and inestimable disability [1, 3]. The pathophysiology of sepsis is perplexing, as some features indicate an overly exuberant inflammatory response, while others reveal relative immunosuppression [2, 4, 5]. These processes may be concurrent, or may be separated by space ( i.e. tissues) and time. Immune dysfunction likely triggers the coagulation abnormalities, endothelial and epithelial barrier disruption, and altered vasoactivity that culminate in multiorgan dysfunction. However, the specific cellular and molecular pathways that are responsible are incompletely understood. These uncertainties surrounding the pathophysiology of sepsis are highlighted by the lack of targeted therapies. With the exception of antibiotics, essentially all of the interventions for sepsis are supportive, rather than directed towards a specific pathophysiology. Thus, targeted therapies to reverse the tissue pathology that occurs during sepsis are needed. A better understanding of the effects of mesenchymal stromal cells on the function of macrophages may open up new therapeutic opportunities for treating sepsis <http://ow.ly/8eRx30j28iH>
Source: European Respiratory Journal
Authors: Maya E. Kotas, Michael A. Matthay
Institution: University of California, San Francisco
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2799745344